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Kalra, Sanjay, and Yatan Pal Singh Balhara. "Insulin Distress." US Endocrinology 14, no. 1 (2018): 27. http://dx.doi.org/10.17925/use.2018.14.1.27.
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Diabetes distress (DD) is a commonly encountered adjustment disorder among persons living with diabetes. This article discusses insulin distress, a subtype of DD, which has distinct characteristics. Insulin distress can be defined as an emotional response to a suggestion to use insulin; characterized by extreme apprehension, discomfort, dejection, or denial; due to a perceived inability to cope with the requirements of insulin therapy. We describe the etiopathogenesis, clinical features and management of insulin distress. They highlight the clinical challenges that insulin distress poses in some persons. Pragmatic suggestions are shared regarding the addressing of insulin distress before or in parallel with insulin prescription.
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Park, Yoonha, and Jae Young Yun. "Visualization Design Suggestion of Artificial Intelligence Based Insulin Prescription Process." Design Convergence Study 20, no. 4 (2021): 1–13. http://dx.doi.org/10.31678/sdc89.1.
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Shehadeh, N., L. Gelertner, S. Blazer, R. Perlman, L. Solovachik, and A. Etzioni. "Importance of insulin content in infant diet: suggestion for a new infant formula." Acta Paediatrica 90, no. 1 (2007): 93–95. http://dx.doi.org/10.1111/j.1651-2227.2001.tb00262.x.
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Laurenti, Marcello C., Chiara Dalla Man, Ron T. Varghese, et al. "Insulin Pulse Characteristics and Insulin Action in Non-diabetic Humans." Journal of Clinical Endocrinology & Metabolism 106, no. 6 (2021): 1702–9. http://dx.doi.org/10.1210/clinem/dgab100.
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Abstract Objective Pulsatile insulin secretion is impaired in diseases such as type 2 diabetes that are characterized by insulin resistance. This has led to the suggestion that changes in insulin pulsatility directly impair insulin signaling. We sought to examine the effects of pulse characteristics on insulin action in humans, hypothesizing that a decrease in pulse amplitude or frequency is associated with impaired hepatic insulin action. Methods We studied 29 nondiabetic subjects on two occasions. On 1 occasion, hepatic and peripheral insulin action was measured using a euglycemic clamp. The deuterated water method was used to estimate the contribution of gluconeogenesis to endogenous glucose production. On a separate study day, we utilized nonparametric stochastic deconvolution of frequently sampled peripheral C-peptide concentrations during fasting to reconstruct portal insulin secretion. In addition to measuring basal and pulsatile insulin secretion, we used approximate entropy to measure orderliness and Fourier transform to measure the average, and the dispersion of, insulin pulse frequencies. Results In univariate analysis, basal insulin secretion (R2 = 0.16) and insulin pulse amplitude (R2 = 0.09) correlated weakly with insulin-induced suppression of gluconeogenesis. However, after adjustment for age, sex, and weight, these associations were no longer significant. The other pulse characteristics also did not correlate with the ability of insulin to suppress endogenous glucose production (and gluconeogenesis) or to stimulate glucose disappearance. Conclusions Overall, our data demonstrate that insulin pulse characteristics, considered independently of other factors, do not correlate with measures of hepatic and peripheral insulin sensitivity in nondiabetic humans.
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Viscarra, Jose A., Cory D. Champagne, Daniel E. Crocker, and Rudy M. Ortiz. "5′AMP-activated protein kinase activity is increased in adipose tissue of northern elephant seal pups during prolonged fasting-induced insulin resistance." Journal of Endocrinology 209, no. 3 (2011): 317–25. http://dx.doi.org/10.1530/joe-11-0017.
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Northern elephant seals endure a 2- to 3-month fast characterized by sustained hyperglycemia, hypoinsulinemia, and increased plasma cortisol and free fatty acids, conditions often seen in insulin-resistant humans. We had previously shown that adipose Glut4 expression and 5′AMP-activated protein kinase (AMPK) activity increase and plasma glucose decreases in fasting seals suggesting that AMPK activity contributes to glucose regulation during insulin-resistant conditions. To address the hypothesis that AMPK activity increases during fasting-induced insulin resistance, we performed glucose tolerance tests (GTT) on early (n=5) and late (n=8)-fasted seal pups and compared adipose tissue expression of insulin signaling proteins, peroxisome proliferator-activated receptor γ (PPARγ), and AMPK, in addition to plasma adiponectin, leptin, cortisol, insulin, and non-esterified fatty acid (NEFA) levels. Fasting was associated with decreased glucose clearance, plasma insulin and adiponectin, and intracellular insulin signaling, as well as increased plasma cortisol and NEFAs, supporting the suggestion that seals develop insulin resistance late in the fast. The expression of Glut4 and VAMP2 increased (52 and 63% respectively) with fasting but did not change significantly during the GTT. PPARγ and phosphorylated AMPK did not change in the early fasted seals, but increased significantly (73 and 50% respectively) in the late-fasted seals during the GTT. Increased AMPK activity along with the reduction in the activity of insulin-signaling proteins supports our hypothesis that AMPK activity is increased following the onset of insulin resistance. The association between increased AMPK activity and Glut4 expression suggests that AMPK plays a greater role in regulating glucose metabolism in mammals adapted to prolonged fasting than in non-fasting mammals.
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Viñals, Clara, Aleix Beneyto, Juan-Fernando Martín-SanJosé, et al. "Artificial Pancreas With Carbohydrate Suggestion Performance for Unannounced and Announced Exercise in Type 1 Diabetes." Journal of Clinical Endocrinology & Metabolism 106, no. 1 (2020): 55–63. http://dx.doi.org/10.1210/clinem/dgaa562.
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Abstract Objective To evaluate the safety and performance of a new multivariable closed-loop (MCL) glucose controller with automatic carbohydrate recommendation during and after unannounced and announced exercise in adults with type 1 diabetes (T1D). Research Design and Methods A randomized, 3-arm, crossover clinical trial was conducted. Participants completed a heavy aerobic exercise session including three 15-minute sets on a cycle ergometer with 5 minutes rest in between. In a randomly determined order, we compared MCL control with unannounced (CLNA) and announced (CLA) exercise to open-loop therapy (OL). Adults with T1D, insulin pump users, and those with hemoglobin (Hb)A1c between 6.0% and 8.5% were eligible. We investigated glucose control during and 3 hours after exercise. Results Ten participants (aged 40.8 ± 7.0 years; HbA1c of 7.3 ± 0.8%) participated. The use of the MCL in both closed-loop arms decreased the time spent <70 mg/dL of sensor glucose (0.0%, [0.0-16.8] and 0.0%, [0.0-19.2] vs 16.2%, [0.0-26.0], (%, [percentile 10-90]) CLNA and CLA vs OL respectively; P = 0.047, P = 0.063) and the number of hypoglycemic events when compared with OL (CLNA 4 and CLA 3 vs OL 8; P = 0.218, P = 0.250). The use of the MCL system increased the proportion of time within 70 to 180 mg/dL (87.8%, [51.1-100] and 91.9%, [58.7-100] vs 81.1%, [65.4-87.0], (%, [percentile 10-90]) CLNA and CLA vs OL respectively; P = 0.227, P = 0.039). This was achieved with the administration of similar doses of insulin and a reduced amount of carbohydrates. Conclusions The MCL with automatic carbohydrate recommendation performed well and was safe during and after both unannounced and announced exercise, maintaining glucose mostly within the target range and reducing the risk of hypoglycemia despite a reduced amount of carbohydrate intake. Register Clinicaltrials.gov: NCT03577158
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Fyles, J. M., M. A. Cawthorne, and S. L. Howell. "The determination of alpha-adrenergic receptor concentration on rat pancreatic islet cells." Bioscience Reports 7, no. 1 (1987): 17–22. http://dx.doi.org/10.1007/bf01122723.
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The selective a2 adrenergic antagonist yohimbine has been shown to prevent the noradrenaline induced inhibition of insulin secretion from isolated rat islets of Langerhans, Binding studies utilizing [3H]yohimbine showed specific binding to dispersed rat islet cells with a Kd of 2.9 nM and receptor concentration of 645 fmols/mg protein. The use of chloroquine to inhibit receptor recycling did not affect binding of the ligand. Binding studies and secretion data are consistent with the suggestion that adrenergic receptors of the α2 sub-type may play a dominant role in the regulation of insulin secretion.
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Burgess, James W., A. Paul Bevan, John J. M. Bergeron, and Barry I. Posner. "Pharmacological doses of insulin equalize insulin receptor phosphotyrosine content but not tyrosine kinase activity in plasmalemmal and endosomal membranes." Biochemistry and Cell Biology 70, no. 10-11 (1992): 1151–58. http://dx.doi.org/10.1139/o92-161.
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Following insulin administration to intact rats, the insulin receptor kinase activity of subsequently isolated cell fractions was significantly augmented. Of interest was the observation that the endosomal insulin receptor tyrosine kinase displayed four- to six-fold greater autophosphorylation activity than that of plasma membrane. Surprisingly, the endosomal insulin receptor tyrosine kinase displayed a decrease in β-subunit phosphotyrosine content compared with that seen in the plasma membrane. These observations prompted the suggestion that insulin receptor tyrosine kinase phosphotyrosine dephosphorylation mediated by an endosome-specific phosphotyrosine phosphatase(s) yields activation of the endosomal insulin receptor tyrosine kinase. In a previous study we examined the effect of subsaturating doses of injected insulin. In this work we evaluated insulin receptor tyrosine kinase activity and phosphotyrosine content in plasma membrane and endosomes after a receptor-saturating pharmacological dose of insulin (150 μg/100 g body weight). At this dose the phosphotyrosine content per receptor was reduced compared with that seen earlier at insulin doses of 1.5 and 15 μg/100 g body weight. Endosomal insulin receptor tyrosine kinase was greater than that seen at the lower nonsaturating insulin doses. Furthermore, endosomal insulin receptor tyrosine kinase activity exceeded that of the plasma membrane, despite retaining about the same phosphotyrosine content per receptor. These data are consistent with the view that insulin receptor tyrosine kinase activity may be regulated by a particular pattern of phosphotyrosine content on the β-subunit wherein both activating and inhibitory phosphotyrosine residues play a role.Key words: insulin receptor tyrosine kinase, autophosphorylation, endosomes, plasma membrane, phosphotyrosine phosphatases.
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Moscardó, Vanessa, José Luis Díez, and Jorge Bondia. "Parallel Control of an Artificial Pancreas with Coordinated Insulin, Glucagon, and Rescue Carbohydrate Control Actions." Journal of Diabetes Science and Technology 13, no. 6 (2019): 1026–34. http://dx.doi.org/10.1177/1932296819879093.
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Background: An artificial pancreas with insulin and glucagon delivery has the potential to reduce the risk of hypo- and hyperglycemia in people with type 1 diabetes. However, a maximum dose of glucagon of 1 mg/d is recommended, potentially still requiring rescue carbohydrates in some situations. This work presents a parallel control structure with intrinsic insulin, glucagon, and rescue carbohydrates coordination to overcome glucagon limitations when needed. Methods: The coordinated controller that combines insulin, glucagon, and rescue carbohydrate suggestions (DH-CC-CHO) was compared with the insulin and glucagon delivery coordinated controller (DH-CC). The impact of carbohydrate quantization for practical delivery was also assessed. An in silico study using the UVA-Padova simulator, extended to include exercise and various sources of variability, was performed. Results: DH-CC and DH-CC-CHO performed similarly with regard to mean glucose (126.25 [123.43; 130.73] vs 127.92 [123.99; 132.97] mg/dL, P = .088), time in range (93.04 [90.00; 95.92] vs 92.91 [90.05; 95.75]%, P = .508), time above 180 mg/dL (4.94 [2.72; 7.53] vs 4.99 [2.93; 7.24]%, P = .966), time below 70 mg/dL (0.61 [0.09; 1.75] vs 0.96 [0.23; 2.17]%, P = .1364), insulin delivery (43.50 [38.68; 51.75] vs 42.86 [38.58; 51.36] U/d, P = .383), and glucagon delivery (0.75 [0.40; 1.83] vs 0.76 [0.43; 0.99] mg/d, P = .407). Time below 54 mg/dL was different (0.00 [0.00; 0.05] vs 0.00 [0.00; 0.16]%, P = .036), although non-clinically significant. This was due to the carbs quantization effect in a specific patient, as no statistical difference was found when carbs were not quantized (0.00 [0.00; 0.05] vs 0.00 [0.00; 0.00]%, P = .265). Conclusions: The new strategy of automatic rescue carbohydrates suggestion in coordination with insulin and glucagon delivery to overcome constraints on daily glucagon delivery was successfully evaluated in an in silico proof of concept.
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Rossello, Xavier, João Pedro Ferreira, John JV McMurray, et al. "Editor’s Choice- Impact of insulin-treated diabetes on cardiovascular outcomes following high-risk myocardial infarction." European Heart Journal: Acute Cardiovascular Care 8, no. 3 (2018): 231–41. http://dx.doi.org/10.1177/2048872618803701.
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Background: Diabetes is associated with poor cardiovascular outcomes, and insulin-treated patients usually have a worse prognosis than non-insulin-treated subjects. The relationship between insulin treatment and outcomes in high-risk myocardial infarction patients has not been described in a large dataset. Methods: To investigate the association between insulin-treated diabetes and long-term cardiovascular outcomes in patients with high-risk myocardial infarction, we used adjusted Cox models to compare cardiovascular mortality and hospitalisation among 28,771 patients grouped by diabetes status and insulin treatment from four randomised clinical trials (VALIANT, EPHESUS, OPTIMAAL, CAPRICORN) of acute myocardial infarction complicated by heart failure and/or left ventricular systolic dysfunction. Results: After an approximately 2-year follow-up, patients with no diabetes (21,386 subjects, 74.3%), non-insulin-treated diabetes (4977 patients, 17.3%) and insulin-treated diabetes (2409 subjects, 8.4%) had an incremental yearly mortality risk (15.8%, 21.3% and 28.1%, respectively). Insulin-treated diabetes patients presented with a higher cardiovascular burden and comorbidities. After adjustment for 18 baseline covariates, patients with non-insulin-treated and insulin-treated diabetes were at higher risk of cardiovascular death (hazard ratio (HR) 1.25, 95% confidence interval (CI) 1.13–1.38 and HR 1.49, 95% CI 1.31–1.69, respectively; P for comparison of non-insulin-treated vs. insulin-treated diabetes =0.016) and cardiovascular hospitalisation (HR 1.33, 95% CI 1.25–1.41 and HR 1.16, 95% CI 1.11–1.22, respectively) compared to patients without diabetes. These results remained consistent after further adjustment for medications and left ventricular ejection fraction. Conclusions: Insulin-treated diabetes patients had higher event rates than diabetes patients taking oral treatments and patients without diabetes. However, insulin-treated diabetes patients had more comorbidities and atherosclerotic disease, precluding any causality suggestion between insulin treatment and outcomes. This high-risk population may require specific and/or more intense cardiovascular protective therapies.
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Costa Rosa, L. F. B. P., Y. Cury, and R. Curi. "Effects of insulin, glucocorticoids and thyroid hormones on the activities of key enzymes of glycolysis, glutaminolysis, the pentose-phosphate pathway and the Krebs cycle in rat macrophages." Journal of Endocrinology 135, no. 2 (1992): 213–19. http://dx.doi.org/10.1677/joe.0.1350213.
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ABSTRACT In the present study the effects of insulin, glucocorticoids and thyroid hormones on macrophage metabolism and function were investigated. The maximum activities of hexokinase, glucose-6-phosphate dehydrogenase, glutaminase and citrate synthase were determined in macrophages obtained from hormonetreated rats and those cultured for a period of 48 h in the presence of hormones. Macrophage phagocytosis was markedly inhibited by dexamethasone and thyroid hormones, remaining unchanged when insulin was added to the culture medium, however. The changes in the enzyme activities caused by hormone treatments of the rats were very similar to those found in culture. Insulin enhanced citrate synthase and hexokinase activities and diminished those of glutaminase and glucose-6-phosphate dehydrogenase. Dexamethasone had a similar effect except on glucose6-phosphate dehydrogenase. The addition of thyroid hormones to the culture medium raised the activities of glutaminase and hexokinase and reduced that of citrate synthase. The results presented support the suggestion that the effects of insulin, glucocorticoids and thyroid hormones on immune and inflammatory responses could well be mediated through changes in macrophage metabolism.. Journal of Endocrinology (1992) 135, 213–219
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Oh, Young Taek, Ki-Sook Oh, Yong Min Choi, et al. "Continuous 24-h nicotinic acid infusion in rats causes FFA rebound and insulin resistance by altering gene expression and basal lipolysis in adipose tissue." American Journal of Physiology-Endocrinology and Metabolism 300, no. 6 (2011): E1012—E1021. http://dx.doi.org/10.1152/ajpendo.00650.2010.
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Nicotinic acid (NA) has been used as a lipid drug for five decades. The lipid-lowering effects of NA are attributed to its ability to suppress lipolysis in adipocytes and lower plasma FFA levels. However, plasma FFA levels often rebound during NA treatment, offsetting some of the lipid-lowering effects of NA and/or causing insulin resistance, but the underlying mechanisms are unclear. The present study was designed to determine whether a prolonged, continuous NA infusion in rats produces a FFA rebound and/or insulin resistance. NA infusion rapidly lowered plasma FFA levels (>60%, P < 0.01), and this effect was maintained for ≥5 h. However, when this infusion was extended to 24 h, plasma FFA levels rebounded to the levels of saline-infused control rats. This was not due to a downregulation of NA action, because when the NA infusion was stopped, plasma FFA levels rapidly increased more than twofold ( P < 0.01), indicating that basal lipolysis was increased. Microarray analysis revealed many changes in gene expression in adipose tissue, which would contribute to the increase in basal lipolysis. In particular, phosphodiesterase-3B gene expression decreased significantly, which would increase cAMP levels and thus lipolysis. Hyperinsulinemic glucose clamps showed that insulin's action on glucose metabolism was improved during 24-h NA infusion but became impaired with increased plasma FFA levels after cessation of NA infusion. In conclusion, a 24-h continuous NA infusion in rats resulted in an FFA rebound, which appeared to be due to altered gene expression and increased basal lipolysis in adipose tissue. In addition, our data support a previous suggestion that insulin resistance develops as a result of FFA rebound during NA treatment. Thus, the present study provides an animal model and potential molecular mechanisms of FFA rebound and insulin resistance, observed in clinical studies with chronic NA treatment.
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Kooistra, T., P. J. Bosma, H. A. M. Töns, A. P. van den Berg, P. Meyer, and H. M. G. Princen. "Plasminogen Activator Inhibitor 1: Biosynthesis and mRNA Level Are Increased by Insulin in Cultured Human Hepatocytes." Thrombosis and Haemostasis 62, no. 02 (1989): 723–28. http://dx.doi.org/10.1055/s-0038-1646891.
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SummaryClinical studies have shown that plasma insulin levels are closely related to plasma plasminogen activator inhibitor 1 (PAI-1) levels. To investigate a possible involvement of hepatocytes we have studied the effect of insulin on PAI-1 production by primary cultures of human hepatocytes. We have isolated human hepatocytes from seven left liver lobes. PAI-1 activity measured in 24 hours conditioned medium varied considerably between the various hepatocyte preparations (from 2.9 to 8.5 units per 5 cm2of cells) possibly as a result of interindividual variability in basal PAI-1 production by hepatocytes from different donors. In all cases, however, the relative extent, time profile and dose-dependency of the insulin-induced increase in PAI-1 synthesis were consistent. Up to about 7 nM, insulin dose-dependently increased both PAI-1 activity and PAI-1 antigen production. The increase in PAI-1 synthesis became measurable between 4 and 8 hours after addition of the hormone, and maximally reached twofold control values. The increase in PAI-1 synthesis could be fully explained by a concomitant increase in PAI-1 mRNA levels. The effect of insulin seems fairly specific for the synthesis of PAI-1: overall protein synthesis and mRNA levels of some control proteins (albumin and fibrinogen) did not markedly change after insulin addition. These results, obtained with primary cultures of human hepatocytes, are fully comparable with those obtained with the hepatocellular carcinoma cell line Hep G2. They strengthen the suggestion that the elevated level of PAI-1 in high insulin plasma might be the result of increased hepatic synthesis of PAI-1.
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Svanberg, E., H. Zachrisson, C. Ohlsson, B. M. Iresjo, and K. G. Lundholm. "Role of insulin and IGF-I in activation of muscle protein synthesis after oral feeding." American Journal of Physiology-Endocrinology and Metabolism 270, no. 4 (1996): E614—E620. http://dx.doi.org/10.1152/ajpendo.1996.270.4.e614.
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The aim was to evaluate the role of insulin and insulin-like growth factor I (IGF-I) in activation of muscle protein synthesis after oral feeding. Synthesis rate of globular and myofibrillar proteins in muscle tissue was quantified by a flooding dose of radioactive phenylalanine. Muscle tissue expression of IGF-I mRNA was measured. Normal (C57 Bl) and diabetic mice (type I and type II) were subjected to an overnight fast (18 h) with subsequent refeeding procedures for 3 h with either oral chow intake or provision of insulin, IGF-I, glucose, and amino acids. Anti-insulin and anti-IGF-I were provided intraperitoneally before oral refeeding in some experiments. An overnight fast reduced synthesis of both globular (38 +/- 3%) and myofibrillar proteins (54 +/- 3%) in skeletal muscles, which was reversed by oral refeeding. Muscle protein synthesis, after starvation/ refeeding, was proportional and similar to changes in skeletal muscle IGF-I mRNA expression. Diabetic mice responded quantitatively similarly to starvation/refeeding in muscle protein synthesis compared with normal mice (C57 Bl). Both anti-insulin and anti-IGF-I attenuated significantly the stimulation of muscle protein synthesis in response to oral feeding, whereas exogenous provision of either insulin or IGF-I to overnight-starved and freely fed mice did not clearly stimulate protein synthesis in skeletal muscles. Our results support the suggestion that insulin and IGF-I either induce or facilitate the protein synthesis machinery in skeletal muscles rather than exerting a true stimulation of the biosynthetic process during feeding.
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Meglasson, M. D., K. M. Smith, D. Nelson, and M. Erecinska. "alpha-Glycerophosphate shuttle in a clonal beta-cell line." American Journal of Physiology-Endocrinology and Metabolism 256, no. 1 (1989): E173—E178. http://dx.doi.org/10.1152/ajpendo.1989.256.1.e173.
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It has been proposed that the alpha-glycerophosphate (alpha-GOP) shuttle plays a crucial role in regulation of glycolysis in beta-cells by linking reoxidation of cytosolic NADH to formation of ATP in the electron transport chain (J. Biol. Chem. 265: 8287, 1981). Direct evidence for this suggestion is still lacking, however. In this work the operation of the alpha-GOP shuttle was investigated in the insulin-secreting cell line HIT-T15. The constituent enzymes of the pathway were found to be present in HIT cells. Flavin-linked alpha-GOP dehydrogenase was associated with the mitochondrial fraction, whereas NAD+-dependent alpha-GOP dehydrogenase was localized in the cytosol. In the presence of amobarbital (used to preserve the function of the alpha-GOP shuttle under conditions where oxidation of NADH by the respiratory chain was blocked), glucose increased insulin secretion, O2 consumption, and the cell [ATP]/[ADP] when compared with amobarbital alone. These results indicate that the alpha-GOP shuttle contributes to ATP generation in HIT cells and that its activation may be necessary for the initiation of insulin secretion by glucose.
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Retnakaran, Ravi, Chang Ye, Philip W. Connelly, Anthony J. Hanley, Mathew Sermer, and Bernard Zinman. "Serum apoA1 (Apolipoprotein A-1), Insulin Resistance, and the Risk of Gestational Diabetes Mellitus in Human Pregnancy—Brief Report." Arteriosclerosis, Thrombosis, and Vascular Biology 39, no. 10 (2019): 2192–97. http://dx.doi.org/10.1161/atvbaha.119.313195.
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Objective: apoA1 (apolipoprotein A-1) is the main lipoprotein associated with HDL (high-density lipoprotein) cholesterol. It was recently reported that intravenous infusion of apoA1 could lower insulin resistance in pregnant rats, leading to the suggestion that apoA1 could provide a target for reducing pregnancy-induced insulin resistance and the risk of gestational diabetes mellitus (GDM) in humans. However, the effects of apoA1 on insulin resistance and risk of GDM in human pregnancy are not known. Thus, we sought to systematically evaluate the relationships of apoA1 with glucose homeostasis and metabolic function in pregnant women. Approach and Results: In this study, 870 pregnant women were recruited in late second trimester and underwent metabolic characterization, including an oral glucose tolerance test on which 214 were diagnosed with GDM. Metabolic characterization included assessment of glucose tolerance, insulin sensitivity/resistance (Matsuda index, homeostasis model assessment of insulin resistance), pancreatic β-cell function, lipids (LDL [low-density lipoprotein] cholesterol, HDL cholesterol, triglycerides, apoB [apolipoprotein B], and apoA1), CRP (C-reactive protein), and adiponectin. Serum apoA1 was strongly correlated with HDL (r=0.79, P <0.0001) and weakly so with adiponectin (r=0.12, P =0.0004) but showed no association with measures of insulin sensitivity/resistance, β-cell function, glycemia, or CRP. There were no significant differences across apoA1 tertiles in mean adjusted Matsuda index ( P =0.24), homeostasis model assessment of insulin resistance ( P =0.08), or area under the glucose curve on the oral glucose tolerance test ( P =0.96). Moreover, there were no differences in risk of GDM across tertiles of apoA1, both before ( P =0.67) and after covariate adjustment ( P =0.78). Conclusions: Serum apoA1 is not associated with insulin resistance or the risk of GDM in human pregnancy.
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Brichard, S. M., L. N. Ongemba, J. Kolanowski, and J. C. Henquin. "The influence of vanadate on insulin counter-regulatory hormones in obese fa/fa rats." Journal of Endocrinology 131, no. 2 (1991): 185–91. http://dx.doi.org/10.1677/joe.0.1310185.
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ABSTRACT Vanadate has been shown to improve glucose homoeostasis in mildly glucose-intolerant and severely insulin-resistant fa/fa rats. The present study examined whether changes in insulin counter-regulatory hormones contribute to this beneficial effect of vanadate. Since oral administration of Na3VO4 caused a decrease in food intake and stopped the increase in body weight, vanadate-treated fa/fa rats were compared with both controls with food available ad libitum and pair-fed rats. Slightly lower plasma glucose levels were maintained in conjunction with markedly lower plasma insulin levels in vanadatetreated rats, and this effect was not simply due to the smaller body weight of the animals. Compared with control rats, treatment with vanadate affected neither basal plasma glucagon levels nor the increase in glucagon levels observed after insulin-induced hypoglycaemia or after i.v. injection of arginine. Compared with pair-fed rats, treatment with vanadate prevented the fall in basal plasma glucagon and its exaggerated rise in response to insulin that mere food restriction produced. Plasma corticosterone levels were high in fa/fa rats. Vanadate and pair-feeding similarly decreased basal plasma levels of corticosterone as well as nocturnal corticosteronuria. Thus the attenuation of the hypercorticism of fa/fa rats results from the reduction in body weight gain rather than from a specific action of vanadate. Vanadate did not influence urinary excretion of noradrenaline, an index of neural sympathetic activity, but prevented the increase in adrenaline excretion, an index of adrenal medulla activity, that was produced by food restriction in pair-fed rats. In conclusion, vanadate administration has no or little specific effects on three major insulin counter-regulatory hormones. This reinforces the suggestion that the beneficial effects of vanadate on glucose homoeostasis in fa/fa rats are mainly due to a correction of insulin resistance in peripheral tissues. Journal of Endocrinology (1991) 131, 185–191
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Oxenkrug, G. F., W. A. Turski, W. Zgrajka, J. V. Weinstock, and P. Summergrad. "Tryptophan-Kynurenine Metabolism and Insulin Resistance in Hepatitis C Patients." Hepatitis Research and Treatment 2013 (September 4, 2013): 1–4. http://dx.doi.org/10.1155/2013/149247.
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Chronic hepatitis C virus (HCV) infection is associated with 50% incidence of insulin resistance (IR) that is fourfold higher than that in non-HCV population. IR impairs the outcome of antiviral treatment. The molecular mechanisms of IR in HCV are not entirely clear. Experimental and clinical data suggested that hepatitis C virus per se is diabetogenic. However, presence of HCV alone does not affect IR. It was proposed that IR is mediated by proinflammatory cytokines, mainly by TNF-alpha. TNF-alpha potentiates interferon-gamma-induced transcriptional activation of indoleamine 2,3-dioxygenase, the rate-limiting enzyme of tryptophan- (TRP-) kynurenine (KYN) metabolism. Upregulation of TRP-KYN metabolism was reported in HCV patients. KYN and some of its derivatives affect insulin signaling pathways. We hypothesized that upregulation of TRP-KYN metabolism might contribute to the development of IR in HCV. To check this suggestion, we evaluated serum concentrations of TRP and KYN and HOMA-IR and HOMA-beta in 60 chronic HCV patients considered for the treatment with IFN-alpha. KYN and TRP concentrations correlated with HOMA-IR and HOMA-beta scores. Our data suggest the involvement of KYN and its metabolites in the development of IR in HCV patients. TRP-KYN metabolism might be a new target for prevention and treatment of IR in HCV patients.
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Vieira, Caroline Evelin Nascimento Kluczynik, Larissa Soares Mariz, Carla Campos Muniz Medeiros, Bertha Cruz Enders, and Alexsandro Silva Coura. "Nursing care in childcare services: Acantose nigricans as a marker for metabolic risk." Revista Latino-Americana de Enfermagem 21, no. 6 (2013): 1220–27. http://dx.doi.org/10.1590/0104-1169.2870.2357.
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OBJECTIVE: to analyze the association between the presence of Acantose nigricans and metabolic changes in overweight adolescents, so as to ascertain the relevance of the identification of this marker in the nursing consultation. METHOD: a cross-sectional study undertaken between April 2009 and April 2010 with 118 adolescents who were service users of the Center for Child Obesity in Campina Grande in the Brazilian State of Paraíba (PB). The presence of Acantose nigricans, and the subjects' anthropometric measurements, were investigated. The following exams were made: insulin, triglycerides, HDL-Cholesterol, Glucose and the homeostatic model of assessment (HOMA-IR). RESULTS: there was association between the presence of Acantose nigricans and participants with insulin resistance (p=0.008), metabolic syndrome (p=0.031), elevated triglycerides (p=0.045) and altered HDL (p=0.002). CONCLUSIONS: the suggestion is supported that the detection/identification of Acantose nigricans may be used in the nursing consultation as a tool for identifying overweight adolescents with greater risk of metabolic changes.
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Trahair, J. F., S. J. Wing, K. J. Quinn, and P. C. Owens. "Regulation of gastrointestinal growth in fetal sheep by luminally administered insulin-like growth factor-I." Journal of Endocrinology 152, no. 1 (1997): 29–38. http://dx.doi.org/10.1677/joe.0.1520029.
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Abstract Fetuses swallow large volumes of amniotic fluid. Absence of swallowing results in gastrointestinal tract (GIT) growth deficits. While it is not yet known to what extent the growth factors present in amniotic fluid are involved in GIT ontogeny, milk-derived growth factors are considered to be important for neonatal growth. Our experiment tested the hypothesis that a luminal growth factor (insulin-like growth factor-I, IGF-I) can sustain or promote GIT growth in utero in a model of gastrointestinal tract growth retardation. Ten-day infusion of either human recombinant IGF-I or vehicle into twin fetal sheep at 80 days gestation via an indwelling esophageal catheter resulted in altered GIT growth. Weight of the forestomach and small intestine increased. Significant histological changes were noted in the proximal small intestine, i.e. the region most exposed to the luminal infusion. Mucosal tissues were reduced in size. While the enterocytes in the proximal small intestine were generally more mature with regard to the ontogeny of the apical endocytic complex (which is responsible for uptake and transport of whole peptides), there were also many abnormal cytological features present. These included the development of large lysosomal-like inclusion bodies and many surfactant-like particles within the apical cytoplasm. Plasma IGF-I levels were on average 20% higher in treated siblings, suggesting that luminal IGF-I crossed the fetal gut and entered blood. IGF-II levels were not significantly affected. These observations are consistent with the suggestion that growth factors, which are present in swallowed amniotic fluid, influence fetal ontogeny. Journal of Endocrinology (1997) 152, 29–38
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El Fouhil, Ahmed F., Aly M. Ahmed, Muhammad Atteya, Raeesa A. Mohamed, Amr S. Moustafa, and Hasem H. Darwish. "An extract from date seeds stimulates endogenous insulin secretion in streptozotocin-induced type I diabetic rats." Functional Foods in Health and Disease 3, no. 11 (2013): 441. http://dx.doi.org/10.31989/ffhd.v3i11.33.
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Background: The efficacy of an extract from date seeds has been tested successfully on the glycemic control of type I diabetes mellitus in rats. A suggestion that date seed extract could stimulate certain cells to differentiate into insulin-secreting cells has been proposed. In order to investigate such a possibility, this study was conducted to measure C-peptide levels in the serum of type 1 diabetic rats treated with date seed extract.Methods: Two hundred rats were divided into 4 groups. Group I served as the control. Group II was given daily ingestions of 10 ml of date seed extract. Groups III and IV were made diabetic by streptozotocin injection and were given daily subcutaneous injections of 3 IU/day of insulin for 8 weeks. Group IV received, in addition, daily ingestions of 10 ml of seed extract. At the end of experiment, blood samples were collected from each rat, and blood glucose and serum C-peptide levels were measured.Results: No significant differences in the means of blood glucose and serum C-peptide levels were observed between groups I (control group) and II (date seed extract-treated control group). Group IV (date seed extract-insulin-treated diabetic group) showed a statistically significant reduction in the mean blood glucose level compared to Group III (insulin-treated diabetic group). The mean serum C-peptide level was significantly higher in group IV compared to group III.Conclusion: Biochemical results suggested an increase in endogenous insulin secretion in the case of type 1 diabetic rats treated with date seed extract, which might be the cause of its hypoglycemic effect.Keywords: Date seed extract; type 1 diabetes; serum C-peptide
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Yudkin, J. S. "Hypertension and coronary artery disease in non-insulin dependent diabetes--cause and effect?" Journal of the American Society of Nephrology 3, no. 4 (1992): S126. http://dx.doi.org/10.1681/asn.v34s126.
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There is a log-linear increase in the risk of coronary heart disease with elevation of levels of blood pressure. Allowing for the phenomenon of regression dilution bias, this corresponds to around a 20 to 25% increase in risk for each 5 to 6 mm Hg elevation in usual diastolic blood pressure. In diabetic subjects, a similar relationship occurs, but of somewhat lesser degree. Recent overviews of therapy suggest that in nondiabetics, reducing blood pressure reverses around 50% of the excess coronary heart disease risk, but this has not yet been conclusively shown in patients with diabetes. The reduction in risk with therapy is a prerequisite to defining the antecedent as a causal influence on outcome, but it is as likely that the incomplete reversibility of excess risk represents other pathways of connection between hypertension and coronary heart disease as a consequent of iatrogenic effects of current treatments. Several alternative mechanisms are outlined, and the suggestion is made that only in the context of randomized controlled studies could the possible benefits on coronary heart disease of agents influencing such mechanisms be assessed.
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Hoelzer, D. R., G. P. Dalsky, N. S. Schwartz, et al. "Epinephrine is not critical to prevention of hypoglycemia during exercise in humans." American Journal of Physiology-Endocrinology and Metabolism 251, no. 1 (1986): E104—E110. http://dx.doi.org/10.1152/ajpendo.1986.251.1.e104.
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We documented stability of plasma glucose concentrations and glucose production and utilization rates, and levels of other metabolic substrates and regulatory factors, during the islet clamp (somatostatin infusion with glucagon and insulin replacement) in the absence of an intervention in five normal humans and further applied this technique to the study of glucoregulation during moderate exercise. Based on previous evidence that sympathochromaffin activation plays a primary role in the prevention of hypoglycemia during exercise, the role of adrenomedullary catecholamines was assessed by exercise (60% of maximum oxygen consumption for 60 min) studies in four bilaterally adrenalectomized, epinephrine-deficient humans under two conditions: control (saline infusion) and islet clamp. Increased glucose utilization and production rates were matched and plasma glucose was unchanged during exercise under both conditions. Thus adrenomedullary catecholamines including epinephrine are not critical to glucoregulation during moderate exercise in humans even when changes in insulin and glucagon are prevented. These findings provide further support for the suggestion that sympathetic neural norepinephrine is the operative catecholamine in the prevention of hypoglycemia during exercise in humans.
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Lowe, Gordon, Gerald Shaper, Peter Whincup, et al. "The effects of different alcoholic drinks on lipids, insulin and haemostatic and inflammatory markers in older men." Thrombosis and Haemostasis 90, no. 12 (2003): 1080–87. http://dx.doi.org/10.1160/th03-04-0221.
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SummaryLight to moderate drinking is associated with lower risk of coronary heart (CHD) than non-drinkers. We have examined the relationships between total alcohol intake and type of alcoholic beverage and several potential biological mechanisms.We carried out the study in 3158 men aged 60-79 years drawn from general practices in 24 British towns with no history of myocardial infarction, stroke or diabetes and who were not on warfarin. Total alcohol consumption showed a significant positive dose-response relationship with high density lipoprotein cholesterol (HDL-C), coagulation factor IX, haematocrit, blood viscosity, and tissue plasminogen (t-PA) antigen, and an inverse dose-response relationship with insulin, fibrinogen, von Willebrand factor (vWF) and triglycerides after adjustment for possible confounders. Total alcohol consumption showed weak associations with plasma viscosity and fibrin D-dimer, and no association with factors VII, VIII, or C-reactive protein (CRP). Wine was specifically associated with lower CRP, plasma viscosity, factor VIII and triglycerides.The findings are consistent with the suggestion that HDL-C in particular but also insulin and haemostatic factors may contribute to the beneficial effect of light to moderate drinking on risk of CHD.Wine has effects that may confer greater protection than other alcoholic beverages.
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Garcia-Leme, J., and Sandra P. Farsky. "Hormonal control of inflammatory responses." Mediators of Inflammation 2, no. 3 (1993): 181–98. http://dx.doi.org/10.1155/s0962935193000250.
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Almost any stage of inflammatory and immunological responses is affected by hormone actions. This provides the basis for the suggestion that hormones act as modulators of the host reaction against trauma and infection. Specific hormone receptors are detected in the reactive structures in inflamed areas and binding of hormone molecules to such receptors results in the generation of signals that influence cell functions relevant for the development of inflammatory responses. Diversity of hormonal functions accounts for recognized pro- and anti-inflammatory effects exerted by these substances. Most hormone systems are capable of influencing inflammatory events. Insulin and glucocorticoids, however, exert direct regulatory effects at concentrations usually found in plasma. Insulin is endowed with facilitatory actions on vascular reactivity to inflammatory mediators and inflammatory cell functions. Increased concentrations of circulating glucocorticoids at the early stages of inflammation results in downregulation of inflammatory responses. Oestrogens markedly reduce the response to injury in a variety of experimental models. Glucagon and thyroid hormones exert indirect anti-inflammatory effects mediated by the activity of the adrenal cortex. Accordingly, inflammation is not only merely a local response, but a hormone-controlled process.
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Mačuks, Ronalds, Ludmila Eņgele, Inta Nuķe, Agnese Sudraba, and Simona Doniņa. "Comparative Analysis of Insulin-like Growth Factor I and Tumour-associated Antigens in Cancer Patients at the Time of Diagnosis." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 63, no. 4-5 (2009): 186–90. http://dx.doi.org/10.2478/v10046-009-0034-5.
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Comparative Analysis of Insulin-like Growth Factor I and Tumour-associated Antigens in Cancer Patients at the Time of Diagnosis Insulin-like growth factor-1 (IGF-1) is a polypeptide hormone with structure similar to insulin. Many experimental data support the suggestion that risk of cancer is higher among persons with raised concentration of IGF-1 and some studies support the role of IGF-1 as a biomarker of increased risk of development of colorectal (CRC) and breast cancer (BC). We have determined IGF-1, CA19-9, CEA, CA72-4 for colorectal, CA15-3 and CEA for breast cancer to clarify utility of IGF-1 as a biomarker of cancer presence at the time of diagnosis. In total, 42 men and 52 women with CRC and 139 women with BC were examined. The cut-off level for IGF-1 concentration in serum was established from results of apparently healthy 27 men and 130 women. An IGF-1 and tumour-associated antigens were detected by chemiluminescence's method using analyser Immulite 2000 (Siemens). Elevated level of IGF-1 was detected in 42.8% of men and 30.7% of women with colorectal cancer. The highest detection rates for CRC using a two biomarker combination were for men as well as for women (57.1% and 57.6%). IGF-1 showed higher detection rates between women with breast cancer in postmenopause vs. women at premenopausal age (33.6% vs. 27.7%). IGF-1 can be used as an additional biomarker for selected colorectal and breast cancer patient groups.
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Sharpe, P. M., P. J. Buttery, and N. B. Haynes. "The effect of manipulating growth in sheep by diet or anabolic agents on plasma cortisol and muscle glucocorticoid receptors." British Journal of Nutrition 56, no. 1 (1986): 289–304. http://dx.doi.org/10.1079/bjn19860108.
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1. The cortisol status (total plasma cortisol concentration, free cortisol concentration, transcortin capacity) and the characteristics of skeletal muscle binding for cortisol and dexamethasone were examined in female lambs either implanted with Zeranol or trenbolone acetate or whose dietary intake was restricted.2. The skeletal muscle glucocorticoid receptor had a high affinity for the glucocorticoid triamcinolone (relative binding affinity 0.85) and cortisol (relative binding affinity 0.51) with virtually no affinity for trenbolone.3. Trenbolone acetate treatment reduced the binding capacity of sheep skeletal muscle for cortisol within 2 d of implantation. The other treatments had little effect except a small reduction in the animals where food intake was restricted. Similarly, binding capacity for dexamethasone was reduced by trenbolone acetate treatment but was not affected by the other treatments. This reduction in trenbolone acetate-treated animals is, at least in part, due to a reduction in glucocorticoid receptors.4. Transcortin capacity was elevated by Zeranol treatment but reduced with diet restriction or trenbolone treatment.5. No support for the suggestion of free cortisol concentration being important in the growth-promoting mechanism of trenbolone or Zeranol was obtained.6. Although insulin concentrations were not significantly altered by treatment (P > 0.05), when combining all the animals there was evidence of a negative correlation between total cortiso1: insulin vaue (P < 0.05) or free cortisol: insulin value and growth rate (P < 0.001). Free cortisol was negatively correlated to growth rate (P < 0.05) and transcortin capacity positively correlated (P < 0.01).
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Eng-Wong, J., S. Chang, S. Hursting, et al. "Premenopausal breast cancer and the association between estrogen receptor status, insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and leptin." Journal of Clinical Oncology 24, no. 18_suppl (2006): 640. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.640.
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640 Background: The IGF pathway and leptin are associated with breast cancer risk in premenopausal women. These proteins are implicated in breast carcinogenesis through their interactions with the estrogen pathway, potentially resulting in specific breast cancer histopathologic subtypes. Methods: Pretreatment serum IGF-I, IGFBP-3 and leptin levels were examined in newly diagnosed premenopausal breast cancer cases to determine whether an association with tumor estrogen receptor status exists. Odds ratios were determined by logistic regression analysis. Likelihood ratio tests for interaction with BMI were conducted. Results: One hundred and eight women were evaluated (mean age 42); 82 were ER positive and 26 were ER negative. 62 were normal weight (BMI<25) and 46 were overweight and obese (BMI≥25). Mean IGF-I, IGFBP-3 and leptin levels did not differ between the ER positive and ER negative tumors. No associations were found between IGF-I, IGFBP-3 or leptin and ER status of tumors overall or by subset analysis in normal weight versus overweight and obese individuals. A suggestion that elevated IGFBP-3 was associated with ER-negative disease did not reach statistical significance. Additionally, normal-weight women with ER-negative disease had higher leptin levels than their normal-weight ER-positive counterparts, although we lacked statistical power to detect an effect of BMI on the association between leptin levels and tumor hormone receptor status. Conclusions: This is the first report examining the IGF pathway and leptin in relation to ER status in premenopausal women with newly diagnosed breast cancer. Our small number of cases suggests a number of intriguing findings that should be evaluated in larger studies. Determining links between ER status and IGFBP-3 and leptin may help better define risk factors and potentially appropriate interventions for ER-negative versus ER-positive breast cancer. No significant financial relationships to disclose.
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McGrattan, PD, AR Wylie, and AJ Bjourson. "A partial cDNA sequence of the ovine insulin receptor gene: evidence for alternative splicing of an exon 11 region and for tissue-specific regulation of receptor isoform expression in sheep muscle, adipose tissue and liver." Journal of Endocrinology 159, no. 3 (1998): 381–87. http://dx.doi.org/10.1677/joe.0.1590381.
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Insulin is as integral and important to the management of metabolism in ruminants as it is in non-ruminants. The suggestion of a lowered ruminant sensitivity and/or responsivity to insulin may relate more to the insulin receptor than to the hormone itself. We screened an ovine cDNA library using degenerate primers and polymerase chain reaction (PCR) to detect and sequence a cDNA portion corresponding to exons 10, 11 and 12 of the human insulin receptor gene in which a 36 base pair (bp) segment (exon 11) is alternatively spliced to produce two distinct receptor isoforms differing in functional characteristics including binding affinity for insulin. The ovine cDNA segment (nucleotides 671 to 770) displayed 84, 84, and 78% nucleotide homology to equivalent segments from the human, rhesus monkey and rat respectively. Reverse transcription PCR (RT-PCR) of selected tissues (liver, m. longissimus dorsi, m. rectus capitis and omental, perirenal and subcutaneous fats) taken at slaughter from three male, pure Dutch Texel lambs (experiment 1) and five male Texel-Greyface crossbred lambs (experiment 2) revealed two mRNA products in each tissue (including spleen; experiment 2 only) corresponding to cDNAs of molecular sizes 161 and 197 bp -- a difference of 36 bp. Sequence alignment showed the 36 bp segment to be homologous to the alternatively spliced exon 11 region of the human insulin receptor gene and to be highly conserved with that from other species. The abundance of the exon 11(+) isoform in the purebred Texel genotype was significantly higher in liver than in perirenal fat and rectus capitis and longissimus dorsi skeletal muscles (P<0.05) and higher also than in subcutaneous and omental fats (P<0.01). There was, however, no difference in the abundance of the exon 11(+) isoform between the individual muscle and fat depots in this sheep genotype. The abundance of the exon 11(+) isoform in the crossbred Texel genotype was significantly higher in liver (P<0. 05) than in the muscles (rectus capitis, P<0.05; longissimus dorsi, P<0.001), all three fats (P<0.001) and spleen (P<0.001). In the crossbred genotype, the abundance of the exon 11(+) isoform was higher in skeletal muscle than in all three fat depots (P<0.001), in which the isoform abundance was similar. Altered ratios of expression of the two products of this alternative splicing event could determine tissue sensitivity and/or responsivity to insulin and provide a mechanism for the management of nutrient partitioning and nutrient utilisation between tissues which is fundamental to the growth of tissues and manipulation of carcass characteristics in meat-producing animals.
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Phillips, Gerald B. "Relationship between serum dehydroepiandrosterone sulfate, androstenedione, and sex hormones in men and women." European Journal of Endocrinology 134, no. 2 (1996): 201–6. http://dx.doi.org/10.1530/eje.0.1340201.
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Phillips GB. Relationship between serum dehydroepiandrosterone sulfate, androstenedione, and sex hormones in men and women. Eur J Endocrinol 1996;134:201–6. ISSN 0804–4643 Previous reports of a correlation between serum dehydroepiandrosterone sulfate (DHEAS) and testosterone in both men and women have led to the suggestion that adrenal and gonadal secretion are related. In the present study, the correlation of DHEAS with testosterone and free testosterone (FT) in both normal men and women was tested. Androstenedione, estradiol, sex hormone binding globulin (SHBG), and insulin were also measured and their correlations determined. All correlations were controlled for age and body mass index. In the men in the study, DHEAS did not correlate with testosterone or FT but correlated strongly with androstenedione. In the women, DHEAS correlated strongly with testosterone, FT. and androstenedione; androstenedione in turn correlated strongly with testosterone and FT. DHEAS showed no correlations with estradiol, SHBG, or insulin in the men or women. The lack of a correlation between DHEAS and testosterone in normal men is consistent with the independent secretion of these hormones by the adrenal and testis, respectively. The finding of a strong DHEAS-testosterone correlation in normal women may be explained by parallel adrenal secretion in response to trophic stimuli, i.e., without invoking an adrenal-gonadal interaction. GB Phillips, Roosevelt Hospital, 428 West 59th Street, New York, NY 10019, USA
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Richelsen, B., S. B. Pedersen, and D. M. Hougaard. "Characterization of antilipolytic action of polyamines in isolated rat adipocytes." Biochemical Journal 261, no. 2 (1989): 661–65. http://dx.doi.org/10.1042/bj2610661.
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The interactions of polyamines with the lipolytic system were studied in isolated rat adipocytes. Spermine, spermidine and putrescine significantly inhibited adenosine deaminase-stimulated lipolysis. An antilipolytic effect of spermine was detectable at a concentration of 0.25 mM (P less than 0.05). At a concentration of 10 mM all three polyamines inhibited the stimulated lipolysis by 50-60% (P less than 0.001). In addition, spermine enhanced the antilipolytic sensitivity of insulin. Spermine (1 mM) decreased the half-maximal inhibitory concentration of insulin from 320 +/- 70 pM to 56 +/- 20 pM (P less than 0.01). The antilipolytic effects and the cyclic-AMP-lowering effects of the polyamines were almost completely prevented in the presence of different phosphodiesterase (PDE) inhibitors (3-isobutyl-1-methylxanthine and RO 20-1724) and, in addition, polyamines had no effect on lipolysis stimulated by dibutyryl cyclic AMP, indicating that polyamines may inhibit lipolysis by activating the PDE enzyme. This latter suggestion was confirmed by demonstrating that spermine (5 mM) significantly enhanced the low-Km PDE enzyme activity (P less than 0.01). Finally, the amounts of polyamines present in isolated adipocytes were measured, and the estimated cytoplasmic concentrations were 0.02 mM (putrescine), 0.86 mM (spermidine), and 1.0 mM (spermine). It is concluded that polyamines may possibly be involved in the physiological regulation of triacylglycerol mobilization in adipocytes.
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Brouwers, Martijn C. G. J., Jacqueline de Graaf, Nynke Simons, et al. "Incidence of type 2 diabetes in familial combined hyperlipidemia." BMJ Open Diabetes Research & Care 8, no. 1 (2020): e001107. http://dx.doi.org/10.1136/bmjdrc-2019-001107.
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ObjectiveFamilial combined hyperlipidemia (FCHL) is common among survivors of a premature myocardial infarction. FCHL patients are characterized by visceral obesity, fatty liver, and insulin resistance. The aim of the present study was to determine the incidence and determinants of type 2 diabetes (T2D) in a longitudinal cohort of FCHL pedigrees.Research design and methodsFCHL patients, their unaffected relatives and spouses included in our baseline cohort in 1998–2005 (n=596) were re-invited to determine the incidence of self-reported T2D (that was confirmed by medical records), used as the primary outcome measure. The Fatty Liver Index (FLI) and Homeostasis Model Assessment Insulin Resistance (HOMA2-IR) were used as markers of fatty liver and insulin resistance, respectively. A subset of the original cohort underwent ultrasound of the liver, and subcutaneous and visceral fat in 2002–2005 (n=275; ‘ultrasound subcohort’).ResultsFollow-up data (median: 15 years) was acquired for 76%. The incidence rate of T2D was significantly higher in FCHL patients compared with spouses (19.2 per 1000 person-years vs 2.8 per 1000 person-years; HR : 6.3, 95% CI: 2.4 to 16.8), whereas no differences were observed between unaffected relatives and spouses (HR: 0.9, 95% CI: 0.3 to 2.6). Cox’s proportional hazard regression analyses showed that baseline HOMA2-IR and FLI≥60, but not waist circumference, BMI, or the FCHL affected state, were independently associated with incident T2D. Similar results were obtained in the ultrasound subcohort (median follow-up: 11 years), in which baseline HOMA2-IR and fatty liver (assessed by ultrasound) were independently associated with incident T2D.ConclusionThis study further corroborates the suggestion that the liver plays a central role in the pathogenesis of cardiometabolic complications in FCHL. It supports periodical screening for T2D in this high-risk population.
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Turk, John, та Sasanka Ramanadham. "The expression and function of a group VIA calcium-independent phospholipase A2 (iPLA2β) in β-cells". Canadian Journal of Physiology and Pharmacology 82, № 10 (2004): 824–32. http://dx.doi.org/10.1139/y04-064.
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Many cells express a Group VIA phospholipase A2, designated iPLA2β, that does not require calcium for activation, is stimulated by ATP, and is sensitive to inhibition by a bromoenol lactone suicide substrate (BEL). Studies in various cell systems have led to the suggestion that iPLA2β has a role in phospholipid remodeling, signal transduction, cell proliferation, and apoptosis. We have found that pancreatic islets, β-cells, and glucose-responsive insulinoma cells express an iPLA2β that participates in glucose-stimulated insulin secretion but is not involved in membrane phos pho lipid remodeling. Additionally, recent studies reveal that iPLA2β is involved in pathways that contribute to β-cell proliferation and apoptosis, and that various phospholipid-derived mediators are involved in these processes. Detailed characterization of the enzyme suggests that the β-cells express multiple isoforms of iPLA2β, and we hypothesize that these participate in different cellular functions.Key words: signalling, apoptosis, isoforms, mass spectrometry.
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Bhaumick, Banani, and R. Marvin Bala. "Differential effects of insulin-like growth factors I and II on growth, differentiation and glucoregulation in differentiating chondrocyte cells in culture." Acta Endocrinologica 125, no. 2 (1991): 201–11. http://dx.doi.org/10.1530/acta.0.1250201.
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Abstract. Insulin-like growth factors I and II have been shown differentially to affect the growth and carbohydrate metabolism of differentiating cartilage developed from mouse embryonic limb buds in organ culture. To gain insight into the relative importance of IGF-I and II actions in different stages of development of cartilage we have established a primary culture of differentiating chondrocytes from mouse embryonic limb buds. Trypsin digested limb bud cells from 9-11 day old mouse embryos differentiated into chondrocytes by 5-7 days in culture. At all stages of differentiation, distinct receptors of IGF-I and II were observed. IGF-I stimulated growth and sulphate incorporation of the non-differentiated and differentiated chondrocytes. IGF-II stimulated growth of the non-differentiated cells and had no effect on growth or sulphate incorporation by the differentiated cells. IGF-II, however, stimulated the glucose uptake by the cells at all stages of differentiation. These data confirm our previous suggestion that IGF-I in cartilage is the regulator of growth and differentiation, while IGF-II may be an important regulator of glucose metabolism in the tissue.
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Easom, R. A., and V. A. Zammit. "Acute effects of starvation and treatment of rats with anti-insulin serum, glucagon and catecholamines on the state of phosphorylation of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase in vivo." Biochemical Journal 241, no. 1 (1987): 183–88. http://dx.doi.org/10.1042/bj2410183.
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The fraction of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase in the dephosphorylated (active) form in rat liver in vivo was measured after various experimental treatments of animals. Intraperitoneal injection of glucose (to raise serum insulin concentrations) into rats 4 h into the light phase (L-4) resulted in a transient (30 min) increase in the expressed (E)/total (T) activity ratio of HMG-CoA reductase without any change in total activity (obtained after complete dephosphorylation of the enzyme). Conversely, intravenous injection of guinea-pig anti-insulin serum into rats 4 h into the dark phase (D-4) significantly depressed the E/T ratio within 20 min. Intravenous injection of glucagon into normal rats at this time point did not affect the degree of phosphorylation of the enzyme, in spite of a 10-fold increase in hepatic cyclic AMP concentration induced by the hormone treatment. A 3-fold increase in the concentration of the cyclic nucleotide induced by adrenaline infusion was similarly ineffective in inducing any change in expressed or total activities of hepatic HMG-CoA reductase. However, when insulin secretion was inhibited, either by the induction of streptozotocin-diabetes or by simultaneous infusion of somatostatin, glucagon treatment was able to depress the expressed activity of HMG-CoA reductase (i.e. it increased the phosphorylation of the enzyme). Therefore insulin appears to have a dominant role in the regulation of the phosphorylation state of hepatic HMG-CoA reductase. In apparent corroboration of this suggestion, short-term 4 h food deprivation of animals before D-4 resulted in a marked decrease in the E/T activity ratio of reductase, which was not affected further by an additional 8 h starvation. By contrast, the total activity of the enzyme was not significantly affected by 4 h starvation, but was markedly diminished after 12 or 24 h starvation. Longer-term starvation also produced a chronic increase in the degree of phosphorylation of the enzyme. These results are discussed in relation to the role of reversible phosphorylation in the control of hepatic HMG-CoA reductase activity in vivo.
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Kemp, E. Helen, Elizabeth A. Waterman, and Anthony P. Weetman. "Immunological pathomechanisms in vitiligo." Expert Reviews in Molecular Medicine 3, no. 20 (2001): 1–22. http://dx.doi.org/10.1017/s1462399401003362.
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Vitiligo is a depigmenting disorder characterised by the loss of melanocytes from the cutaneous epidermis. Although the exact aetiology of vitiligo has not yet been established, the abnormal immune responses frequently observed in vitiligo patients have led to the suggestion that, in some cases, the condition has an autoimmune component. Briefly, circulating autoantibodies and autoreactive T cells that recognise pigment cell antigens have been detected in the sera of a significant proportion of vitiligo patients compared with healthy individuals. In addition, vitiligo is often associated with other disorders that have an autoimmune origin, including Hashimoto's thyroiditis, Graves' disease, type 1 insulin-dependent diabetes mellitus and Addison's disease. Furthermore, effective use of immunosuppressive therapies to treat vitiligo, the association of vitiligo with certain major histocompatibility complex antigens, and evidence from animal models of the disease have all added credence to the hypothesis that immune reactions play a role in vitiligo pathogenesis. This review presents and discusses the evidence for immunological pathomechanisms in vitiligo.
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Ravi Kumar, Ravi Varma BH, Vijayabhasker V, and Avinash Kulkarni. "An Analytical Study on Associated Type-II Diabetic Mellitus with ABO Rhesus Blood Groups." International Journal of Research in Pharmaceutical Sciences 11, SPL4 (2020): 264–68. http://dx.doi.org/10.26452/ijrps.v11ispl4.3782.
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Diabetes mellitus (DM) is a metabolic disorder categorized by hyperglycemia subsequent that faults of insulin emission and/or insulin cellular resistance and is the fore most reason for disease and mortality. The ABO blood collections frequently related by numerous illnesses through one blood group added repeatedly grown by the patients of a specific disease. The aim of this learning is to regulate the association among ABO & Rhesus blood groups and Type-2 diabetes mellitus in the local populace of Visakhapatnam. The present study is a hospital depended on the cross-sectional, case-control study, directed over a phase of six months in out-patient units of endocrinology department of a tertiary care hospital. An entire of 332 patients by Type-II DM and 200 age and sex harmonized healthy controls were included. In cases group, out of 332 patients 174(52.4%) were males (vs 113(56.5%) controls) and 158(47.5%) were females (vs 87(43.5%) controls) and about 289(87.04%) patients were found to be Rh+ve type (vs 178(89%) controls). About 91(27.4%) were found to be B-positive (vs 28(14%) controls), 87(26.2%) were O-positive (vs 69( 34.5%) controls ), and 73(22%) are A-positive (vs 62(31%) controls), 38(11.45%) are AB-positive (vs 19(9.5%) controls) , 14(4.2%) are O-negative(vs 3(1.5%) controls), 11(3.3%) are A-negative(vs 10(5%) controls),10(3.0%) are AB-negative(vs 3(1.5%) controls), 8(2.4%) are B-negative(vs 6(3%) controls). There is a suggestion among ABO antigens and Rhesus blood groups by Type-II DM. DM is more common in patients with B blood group and Rh-Positive.
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Kos, Katarina, Alison L. Harte, Nancy F. da Silva, et al. "Adiponectin and Resistin in Human Cerebrospinal Fluid and Expression of Adiponectin Receptors in the Human Hypothalamus." Journal of Clinical Endocrinology & Metabolism 92, no. 3 (2007): 1129–36. http://dx.doi.org/10.1210/jc.2006-1841.
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Abstract Context: The adipokine leptin has critical importance in central appetite regulation. In contrast to some suggestion of adiponectin influencing energy homeostasis in rodents, there is no evidence for adiponectin or resistin entering the human blood-brain barrier. Objective: The objective was to establish the presence of adiponectin or resistin in human cerebrospinal fluid (CSF) and to compare their distribution with leptin. Furthermore, we wished to examine the expression of the adiponectin receptors 1 and 2 (AdipR1, AdipR2) in the human hypothalamus. Methods: For this purpose, serum and CSF samples were collected from 20 men and 19 women matched for age [men, 69.8 ± 8.6 yr (mean ± sd); women, 69.4 ± 4.3 yr] and BMI (men, 29.4 ± 3.4 kg/m2; women, 27.3 ± 4.8 kg/m2) undergoing elective surgery under spinal anesthesia. Results: Adiponectin was identified in CSF with levels 1000-fold less than serum, whereas resistin and leptin levels were 100-fold less. Unlike their serum levels, adiponectin CSF levels showed no gender difference or correlation with insulin resistance, which is similar to resistin CSF levels. The adiponectin and leptin CSF/serum ratios in our study exhibit the same pattern of gender-specific BMI association with inverse correlation in women (r = −0.61; P = 0.02) and no correlation in men (r = 0.026; P = not significant). Furthermore, immunostaining established AdipR1 and -2 in the hypothalamus and increased AdipR2 expression in the paraventricular nucleus, which is involved in energy regulation. Conclusion: In summary, our findings show both the presence of adiponectin and resistin in human CSF, with no effect of insulin resistance on CSF levels. The CSF entry of adiponectin and leptin in women appears to be impaired in obesity.
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Badrujamaludin, Asep, M. Budi Santoso, and Deipa Nastrya. "Hubungan aktivitas fisik dengan kejadian neuropati diabetik pada penderita diabetes mellitus Tipe 2." Holistik Jurnal Kesehatan 15, no. 2 (2021): 176–86. http://dx.doi.org/10.33024/hjk.v15i2.3624.
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The association of physical activity in people with type 2 diabetes and peripheral neuropathyBackground: Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia due to the pancreas not producing enough insulin or the insulin produced cannot be used properly. According to data from International Diabetic Federation in 2019, Indonesia ranks 7th in the world with 10.7 million people with diabetes mellitus. There are pillars of diabetes mellitus management one of which is physical activity. Diabetic neuropathy is one of the complications of type 2 DM that can occur if the diabetes is not managed properly.Purpose: To determine the association of physical activity in people with type 2 diabetes and peripheral neuropathyMethod: Quantitative research and correlation analytic with cross-sectional design. Sampling took by a purposive sampling of 103 respondents at Cigugur Public Health Center, Collecting data using questionnaires, and nalyzed univariate (frequency distribution) and bivariate using Chi-Square test.Results: Finding most of the respondents had low physical activity (71.8%), and most of them had diabetic neuropathy (76.7%) with a p-value = 0,000Conclusion: There is a relationship between physical activity and peripheral neuropathy, suggestion for people with diabetes mellitus to do regular physical activity to control blood sugar levels and prevent complications of diabetic neuropathy and aerobic physical exercises such as walking, relaxed cycling, jogging, and swimming.Keywords: Physical activity; Patient; Type 2 diabetes; Peripheral neuropathyPendahuluan: Diabetes melitus (DM) adalah penyakit metabolik yang ditandai oleh hiperglikemia akibat pankreas tidak memproduksi cukup insulin atau insulin yang diproduksi tidak dapat digunakan dengan baik. Menurut data dari Internasional Diabetic Ferderation pada tahun 2019, Indonesia menempati urutan ke 7 di dunia dengan jumlah penderita diabetes melitus sebanyak 10,7 juta penderita. Terdapat pilar penatalaksanaan diabetes mellitus salah satunya adalah aktivitas fisik. Neuropati diabetik merupakan salah satu komplikasi dari DM tipe 2 yang dapat terjadi jika DM tersebut tidak dikelola dengan baikTujuan: Untuk mengetahui hubungan aktivitas fisik dengan kejadian neuropati diabetik pada penderita DM tipe 2Metode: Penelitian analitik korelasi dengan desain cross sectional. Teknik sampling yang digunakan purposive sampling. Jumlah sampel pada penelitian ini yaitu 103 responden. Teknik pengumpulan data menggunakan kuesioner. Data dianalisis secara univariat (distribusi frekuensi) dan bivariat menggunakan uji Chi-Square.Hasil: Sebagian besar dari responden memiliki aktivitas fisik ringan (71,8%), dan sebagian besar mengalami neuropati diabetik (76,7%) dengan p-value = 0.000.Simpulan: Terdapat hubungan antara aktivitas fisik dengan kejadian neuropati diabetik pada penderita DM tipe 2. Saran bagi penderita diabetes mellitus untuk melakukan aktivitas fisik teratur untuk mengontrol kadar gula darah dan mencegah terjadinya komplikasi neuropati diabetik serta latihan jasmani yang bersifat aerobik seperti jalan kaki, bersepeda santai, jogging, dan berenang.
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Vita Gloria, Christine, Yuyun Priwahyuni, M. Dedi Widodo, and Suci Fanesa. "DETERMINAN KEJADIAN DIABETES MELITUS TIPE 2 DI WILAYAH KERJA PUSKESMAS PAYUNG SEKAKI." Jurnal Penelitian Kesmasy 2, no. 1 (2019): 40–44. http://dx.doi.org/10.36656/jpksy.v2i1.156.
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Diabetes Mellitus is abnormality of insulin hormone that is marked with high blood glucose levels. In indonsia, total of diabetes mellitus sufferer in 2000 is 8,4 million (7,8%) peoples and expected in 2030 will reached untll 21,3 million (9,1%) people. Diabetes mellitus case in work area of Public Health Centre (PHC) Payung Sekaki Pekanbaru City In 2017 is 1.798 (2,3%). This research purpose is to knowing determinants case of diabetes melliitus type 2 in work area PHC Payung Sekaki Pekanbaru City. This research method is quantitative with research type is observational analysis and this design research is case control. Technique Sampling which is used is Non Probability and Quota Sampling technique. Analysis of data what done is univariat and bivariat wit Chi Square test. The result research show that, there are corelation among age, obesity, exercise, eating pattern with Diabetes Mellitus Type 2 case, andthere is no corelation between family support with Diabetes Mellitus Type 2case. Suggestion for PHC, to do socialization about managed healthy life pattern, keep the ideal body weight, also helding the healthy gymnastics program in PHC in the morning as 3 times in a week.
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Rojas, Milagros, Mervin Chávez-Castillo, Daniela Pirela, et al. "Metabolic Syndrome: Is It Time to Add the Central Nervous System?" Nutrients 13, no. 7 (2021): 2254. http://dx.doi.org/10.3390/nu13072254.
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Metabolic syndrome (MS) is a set of cardio-metabolic risk factors that includes central obesity, hyperglycemia, hypertension, and dyslipidemias. The syndrome affects 25% of adults worldwide. The definition of MS has evolved over the last 80 years, with various classification systems and criteria, whose limitations and benefits are currently the subject of some controversy. Likewise, hypotheses regarding the etiology of MS add more confusion from clinical and epidemiological points of view. The leading suggestion for the pathophysiology of MS is insulin resistance (IR). IR can affect multiple tissues and organs, from the classic “triumvirate” (myocyte, adipocyte, and hepatocyte) to possible effects on organs considered more recently, such as the central nervous system (CNS). Mild cognitive impairment (MCI) and Alzheimer’s disease (AD) may be clinical expressions of CNS involvement. However, the association between MCI and MS is not understood. The bidirectional relationship that seems to exist between these factors raises the questions of which phenomenon occurs first and whether MCI can be a precursor of MS. This review explores shared pathophysiological mechanisms between MCI and MS and establishes a hypothesis of a possible MCI role in the development of IR and the appearance of MS.
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Duan, C., T. Noso, S. Moriyama, H. Kawauchi, and T. Hirano. "Eel insulin: isolation, characterization and stimulatory actions on [35S]sulphate and [3H]thymidine uptake in the branchial cartilage of the eel in vitro." Journal of Endocrinology 133, no. 2 (1992): 221–30. http://dx.doi.org/10.1677/joe.0.1330221.
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ABSTRACT Our previous studies have shown that mammalian and salmon insulins stimulate sulphate uptake by cultured eel cartilage, suggesting the possible involvement of insulin in the regulation of cartilage matrix synthesis. In the present study, homologous eel insulin was isolated and characterized, and its effects on cartilage matrix synthesis and DNA synthesis were examined in vitro. Insulin was extracted from eel pancreas with acid–ethanol, and subsequently purified by isoelectric precipitation at pH 5·3, gel filtration on Sephadex G-50, and reversed-phase high-performance liquid chromatography. The amino acid composition and complete sequence (50 residues) of eel insulin revealed high homology to teleostean and mammalian insulins. The isolated eel insulin produced a more pronounced and longer lasting hypoglycaemic effect than bovine insulin in the eel. Homologous eel insulin, like bovine insulin-like growth factor (IGF-I) and insulin, stimulated sulphate uptake by cultured eel cartilage in a dose-dependent manner (16–1000 ng/ml). Combination experiments using maximal concentrations of bovine IGF-I (250 ng/ml) and increasing amounts of eel insulin (10–250 ng/ml) showed no additive effects of insulin on sulphate uptake, suggesting that insulin and IGF-I may share a common mechanism(s) of action. Eel insulin and bovine IGF-I also enhanced thymidine incorporation by eel cartilage in a dose-dependent manner (4–1000 ng/ml); eel insulin was equipotent with bovine IGF-I. These results suggest that insulin, like IGF-I, may exert direct growth-promoting actions in branchial cartilage of the eel. Journal of Endocrinology (1992) 133, 221–230
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Catherine, Bell, Cropper Julie, Stephenson Tracey, Campbell Fiona, and Hattersley Andrew. "SP6 Use of glibenclamide in neonatal diabetes." Archives of Disease in Childhood 103, no. 2 (2018): e1.48-e1. http://dx.doi.org/10.1136/archdischild-2017-314584.6.
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SituationJJ is a neonate born with diabetes due to a suspected KCNJ11 mutation which was later confirmed by genetic testing. The KCNJ11 mutation results in the patient being unable to produce insulin due to an inability to close a potassium dependent ATP channel required for the process. Prior to the administration of an intravenous (IV) insulin infusion JJ’s blood glucose levels reached 17 mmol/L. A plan for long term management of this patient’s condition was required before discharge.BackgroundUntreated or uncontrolled neonatal diabetes can result in severe complications such as reduced renal function or intra-ventricular haemorrhage therefore prompt and continued management of blood glucose levels is essential.OutcomeOptions for JJ’s long term management were considered by the paediatric diabetes multi-disciplinary team (MDT) following the suggestion of use of a sulphonylurea. Prior experience of its use had been found to be the most effective therapy in patients with KCNJ11 mutations.1 Continuation of IV therapy was unsuitable because of poor IV access and challenging monitoring requirements. Subcutaneous therapy was dismissed due to variability and unpredictability of pharmacokinetics and pain on injection in a neonate. Expert advice was sought from Exeter University specialists who recommended the use of glibenclamide specifically. A literature search described its use in a 3 month old at a dose of 0.1 mg/kg/day.1 A reference discussed 3 extemporaneous formulations and demonstrated chemical stability2 but with rapid settling and poor dose uniformity. It was decided that an extemporaneous product was also unsuitable due to potential for variation of formulation between primary and secondary care. As glibenclamide is insoluble in water a suspension was required to ensure uniformity of distribution of the drug and therefore reliable dosing. An acceptable product manufactured by a specials company as a suspension was identified and product information requested to determine potential suitability for use in neonates with regards to excipients.JJ was discharged at 2 weeks of age with frequent planned review by the MDT. His blood glucose levels were stable, although there were some instances of hypoglycaemia post-dose and hyperglycaemia pre-dose therefore the dose was eventually reduced to 0.04 mg/kg/day and split into 3 divided doses to prevent this. He remains well, is showing normal growth and development with stable blood glucose results since the dose amendment.Lessons learntSulphonylureas close the potassium dependent channel independently of ATP that patients with KCNJ11 mutations cannot. This results in the ability of these patients to produce insulin endogenously whereas previously they would have required full insulin supplementation. Prompt and clear MDT communication and the use of glibenclamide in a neonate enabled discharge due to improved blood glucose levels within 48 hours of initiation.ReferencesPearson ER, et al. Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutation. New England Journal of Medicine 2006;355(5):467–77.Di Folco U, et al. Stability of three different galenic liquid formulations compounded from tablet containing glibenclamide. Journal of Nutritional Therapeutics 2012;1:152–160.
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DÜFER, Martina, Peter KRIPPEIT-DREWS, Linas BUNTINAS, Detlef SIEMEN та Gisela DREWS. "Methyl pyruvate stimulates pancreatic β-cells by a direct effect on KATP channels, and not as a mitochondrial substrate". Biochemical Journal 368, № 3 (2002): 817–25. http://dx.doi.org/10.1042/bj20020657.
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In pancreatic β-cells, methyl pyruvate is a potent secretagogue and is widely used to study stimulus—secretion coupling. In contrast with pyruvate, which barely stimulates insulin secretion, methyl pyruvate was suggested to act as an effective mitochondrial substrate. We show that methyl pyruvate elicited electrical activity in the presence of 0.5mM glucose, in contrast with pyruvate. Accordingly, methyl pyruvate increased the cytosolic free Ca2+ concentration after an initial decrease, similar to glucose. The initial decrease was inhibited by thapsigargin, suggesting that methyl pyruvate stimulates ATP production. This assumption is supported by the observation that methyl pyruvate hyperpolarized the mitochondrial membrane potential, similar to glucose. However, in contrast with glucose, methyl pyruvate even slightly decreased NAD(P)H autofluorescence and did not influence ATP production or the ATP/ADP ratio. This observation questions the suggestion that methyl pyruvate acts as a powerful mitochondrial substrate. The finding that methyl pyruvate directly inhibited a cation current across the inner membrane of Jurkat T-lymphocyte mitochondria suggests that this metabolite may increase ATP production in β-cells by activating the respiratory chains without providing reduction equivalents. We conclude that this mechanism may account for a slight and transient increase in ATP production. We further show that methyl pyruvate inhibited the KATP current measured in the standard whole-cell configuration, an effect that was at least partly antagonized by diazoxide. Accordingly, single-channel currents in inside-out patches were blocked by methyl pyruvate. We conclude that inhibition of KATP channels, and not activation of metabolism, mediates the induction of electrical activity in pancreatic β-cells by methyl pyruvate.
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Brackley, Karyn. "The cerebral hypometabolism model of Alzheimer's disease explored: can a ketogenic diet improve cognition in Alzheimer's disease? A review of the literature." British Journal of Neuroscience Nursing 17, no. 3 (2021): 95–103. http://dx.doi.org/10.12968/bjnn.2021.17.3.95.
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Background: Much research supports the emerging theory that Alzheimer's disease originates from a pathological cerebral metabolic disturbance in glucose metabolism, analogous to insulin resistance in type 2 diabetes. This has led to the theory that ketone bodies may provide an alternative neuronal fuel, correcting, in part, the neuronal energy deficiency and improving cognition in Alzheimer's disease. Aims: To evaluate the literature of human studies on the effectiveness of improving cognition in Alzheimer's disease through a low-carbohydrate diet or administration of exogenous ketones. Methods: A literature review was conducted, with the PRISMA guidelines used to guide this review. The PICO (Population, Intervention, Comparison, Outcome) concept tool was used to search for terms generated through background research. Full-text, peer-reviewed English articles from SocINDEX, Medline, CINAHL, PsychInfo and ScienceDirect were selected, using exclusion and inclusion criteria. Six human studies in which cognition was assessed following a low-carbohydrate diet or administration of exogenous ketones were evaluated. Findings: Some cognitive improvements were demonstrated in all studies in participants with mild-moderate Alzheimer's disease, but not in all cognitive tests and not at all time points. Cognitive improvements returned to baseline after the intervention. Two studies included genetic data and found that cognitive improvement was most notable in those without an E4 allele. Conclusions: This review provides some preliminary support for the potential therapeutic use of ketones in Alzheimer's disease. However, considerable future research is needed, as this is a relatively novel research area. The findings support the suggestion of a gene-environment interaction in the aetiology of Alzheimer's disease, and may contribute to an understanding of how the E4 allele is linked to the pathology of Alzheimer's disease. This review provides suggestions for improving screening for Alzheimer's disease from a nursing perspective—for example, by screening for risk factors, such as hyperinsulinemia and reduced cerebral metabolic rate of glucose.
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Trinick, T. R., M. F. Laker, D. G. Johnston, M. Keir, K. D. Buchanan, and K. G. M. M. Alberti. "Effect of guar on second-meal glucose tolerance in normal man." Clinical Science 71, no. 1 (1986): 49–55. http://dx.doi.org/10.1042/cs0710049.
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1. Whole body glucose turnover and absorption of a 50 g glucose drink was studied in six healthy volunteers on two occasions, 4 h after a ‘breakfast’ of 50 g of glucose, mixed on one occasion with 20 g of guar gum. 2. Plasma glucose concentrations were significantly reduced with guar gum compared with those obtained without guar gum (P < 0.0001). 3. Whole body glucose turnover studied by an intravenous primed dose constant infusion technique using d-[3-3H]glucose showed no significant difference between the two groups: 353 ± 15 mmol with guar and 350 ± 9 mmol without guar. 4. Total oral glucose absorption, followed with a D-[1-14C]glucose tracer, was significantly decreased by guar treatment, being 219 ± 3 mmol with guar and 239 ± 5 mmol without guar (P < 0.05). 5. Serum insulin levels were lowered by guar treatment (P<0.05) while those of C-peptide, gastric inhibitory polypeptide, glucagon, Cortisol and pancreatic polypeptide did not differ significantly. 6. Blood lactate concentrations were raised in the guar treated group (P < 0.05) whereas pyruvate, alanine, glycerol and 3-hydroxybutyrate concentrations did not differ significantly. 7. These results support the suggestion that guar improves second-meal tolerance to glucose by decreasing absorption.
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Barrett, Eugene J., Hong Wang, Charles T. Upchurch, and Zhenqi Liu. "Insulin regulates its own delivery to skeletal muscle by feed-forward actions on the vasculature." American Journal of Physiology-Endocrinology and Metabolism 301, no. 2 (2011): E252—E263. http://dx.doi.org/10.1152/ajpendo.00186.2011.
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Insulin, at physiological concentrations, regulates the volume of microvasculature perfused within skeletal and cardiac muscle. It can also, by relaxing the larger resistance vessels, increase total muscle blood flow. Both of these effects require endothelial cell nitric oxide generation and smooth muscle cell relaxation, and each could increase delivery of insulin and nutrients to muscle. The capillary microvasculature possesses the greatest endothelial surface area of the body. Yet, whether insulin acts on the capillary endothelial cell is not known. Here, we review insulin's actions at each of three levels of the arterial vasculature as well as recent data suggesting that insulin can regulate a vesicular transport system within the endothelial cell. This latter action, if it occurs at the capillary level, could enhance insulin delivery to muscle interstitium and thereby complement insulin's actions on arteriolar endothelium to increase insulin delivery. We also review work that suggests that this action of insulin on vesicle transport depends on endothelial cell nitric oxide generation and that insulin's ability to regulate this vesicular transport system is impaired by inflammatory cytokines that provoke insulin resistance.
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Ader, M., and R. N. Bergman. "Peripheral effects of insulin dominate suppression of fasting hepatic glucose production." American Journal of Physiology-Endocrinology and Metabolism 258, no. 6 (1990): E1020—E1032. http://dx.doi.org/10.1152/ajpendo.1990.258.6.e1020.
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Insulin may suppress hepatic glucose production directly, or indirectly via suppression of release of gluconeogenic substrates from extrasplanchnic tissues. To compare these mechanisms, we performed insulin dose-response experiments in conscious dogs at euglycemia, during somatostatin infusion, and intraportal glucagon replacement. Insulin was sequentially infused either intraportally (0.05, 0.20, 0.40, 1.0, 1.4, and/or 3.0; protocol I) or systemically at half the intraportal rate (0.025, 0.10, 0.20, 0.50, 0.70, and/or 1.5 mU.min-1.kg-1; protocol II). Exogenous glucose infused during clamps was labeled with 3-[3H]glucose (2 microCi/g) to prevent a fall in plasma specific activity (P greater than 0.2) that may have contributed to previous underestimations of hepatic glucose output (HGO). Portal insulins were up to threefold higher during intraportal infusion, but peripheral insulin levels were not different between the intraportal and systemic protocols [7 +/- 5 vs. 9 +/- 1, 12 +/- 4 vs. 13 +/- 6, 16 +/- 3 vs. 27 +/- 5, 70 +/- 23 vs. 48 +/- 8, 83 +/- 3 vs. 86 +/- 21, and 128 vs. 120 +/- 14 microU/ml for paired insulin doses; P greater than 0.06 by analysis of variance (ANOVA)]. Despite higher portal insulin levels in protocol I, HGO suppression was equivalent in the two protocols when systemic insulin was matched, from 3.3 +/- 0.1 to near-total suppression at 0.3 mg.min-1.kg-1 at the highest insulin infusion rate (3.0 mU.min-1.kg-1; P less than 0.0001) with intraportal insulin, from 2.9 +/- 0.8 to -0.8 +/- 0.2 mg.min-1.kg-1 in protocol II (P less than 0.001). Suppression of HGO was similar at matched systemic insulin, regardless of portal insulin, suggesting the primacy of insulin's action on the periphery in its restraint of hepatic glucose production.
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Ortega-Pacheco, Diego, María Marcela Jiménez-Pérez, Jeanet Serafín-López, Juan Gabriel Juárez-Rojas, Arturo Ruiz-García, and Ursino Pacheco-García. "Vanadyl Sulfate Effects on Systemic Profiles of Metabolic Syndrome in Old Rats with Fructose-Induced Obesity." International Journal of Endocrinology 2018 (December 25, 2018): 1–12. http://dx.doi.org/10.1155/2018/5257216.
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Background. Currently, energy obtained from hypercaloric diets has been part of the obesity and type 2 diabetes mellitus (T2DM) epidemics from childhood to old age. Treatment alternatives have been sought from plants, minerals, and trace elements with metabolic effects. Vanadyl sulfate (VS) has been investigated as a hypoglycemic compound in animal and human studies showing effective insulin-mimetic properties. This characteristic encompasses several molecules that have beneficial pleiotropic effects. The aim was to determine the antiobesity, hypoglycemic, and hypolipidemic effects of VS on fructose-induced metabolic syndrome in aged rats. Material and Methods. Five groups of male Wistar rats were made, each with six rats: two groups with normal diet (ND) and three with high-fructose diet (HFD). The first ND group was treated with saline solution (SS), the second with VS; treatment for HFD groups was in the first group with SS, second with VS, and third with metformin. Weight, body mass index (BMI), blood glucose, and lipidic profile were measured; water, food, fructose and energy consumption were also determined. All parameters were compared among groups. Results and Discussion. Although obese rats treated with VS presented anorexia, oligodipsia, and a marked weight loss in the first two weeks. They recovered food and water intake in the third week with a slow recovery of some weight weeks later. VS normalized blood glucose level and decreased triglyceride and insulin levels in obese rats. These results suggest that vanadyl sulfate shows antiobesity, hypoglycemic, and hypolipidemic properties in old obese rats and could be useful as an alternative, additional, and potent preventive treatment for obesity and T2DM control in elderly obese and poorly controlled diabetic patients. Conclusion. VS could play an important role in the treatment of metabolic syndrome, contributing to a decrease in obesity and T2DM, through different ways, such as euglycemia, satiety, weight loss, and lipid profile optimization, among others. However, more research is needed to confirm this suggestion.
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Yeh, J. K., J. F. Aloia, M. Chen, N. Ling, H. C. Koo, and W. J. Millard. "Effect of growth hormone administration and treadmill exercise on serum and skeletal IGF-I in rats." American Journal of Physiology-Endocrinology and Metabolism 266, no. 1 (1994): E129—E135. http://dx.doi.org/10.1152/ajpendo.1994.266.1.e129.
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Growth factors may be mediators of local and systemic factors that enhance bone formation. This study examined the effect of treadmill exercise and ovine growth hormone administration on levels of insulin-like growth factor I (IGF-I) in serum (ng/ml), long bone, and vertebrae and on bone formation rate. Forty female rats were divided into four groups: control; exercise (17 m/min, 1 h/day); growth hormone (0.05 mg.100 g-1.day-1); growth hormone plus exercise. After 9 wk of study, the serum levels of IGF-I were higher in the intervention groups than in the control group; however, the IGF-I concentration and the periosteal bone formation rate in the long bone were significantly higher only in the exercised rats. The IGF-I concentration and the cancellous bone formation rate in the vertebrae did not differ among the experimental groups. The vertebral and long bone formation rate were correlated with bone concentrations of IGF-I. Serum levels of IGF-I were also correlated with serum osteocalcin and the long bone formation but not with the vertebral bone formation. The association of bone formation with serum and bone IGF-I supports the suggestion that IGF-I is one of the growth factors that regulate bone formation, in particular as a mediator of the response of bone to exercise.