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Journal articles on the topic 'Glucose tolerance/ intolerance'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Szlapinski, Sandra K., Anthony A. Botros, Sarah Donegan, et al. "Altered pancreas remodeling following glucose intolerance in pregnancy in mice." Journal of Endocrinology 245, no. 2 (2020): 315–26. http://dx.doi.org/10.1530/joe-20-0012.

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Gestational diabetes mellitus increases the risk of dysglycemia postpartum, in part, due to pancreatic β-cell dysfunction. However, no histological evidence exists comparing endocrine pancreas after healthy and glucose-intolerant pregnancies. This study sought to address this knowledge gap, in addition to exploring the contribution of an inflammatory environment to changes in endocrine pancreas after parturition. We used a previously established mouse model of gestational glucose intolerance induced by dietary low protein insult from conception until weaning. Pancreas and adipose samples were

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Mangiafico, Salvatore P., Shueh H. Lim, Sandra Neoh, et al. "A primary defect in glucose production alone cannot induce glucose intolerance without defects in insulin secretion." Journal of Endocrinology 210, no. 3 (2011): 335–47. http://dx.doi.org/10.1530/joe-11-0126.

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Increased glucose production is associated with fasting hyperglycaemia in type 2 diabetes but whether or not it causes glucose intolerance is unclear. This study sought to determine whether a primary defect in gluconeogenesis (GNG) resulting in elevated glucose production is sufficient to induce glucose intolerance in the absence of insulin resistance and impaired insulin secretion. Progression of glucose intolerance was assessed in phosphoenolpyruvate carboxykinase (PEPCK) transgenic rats, a genetic model with a primary increase in GNG. Young (4–5 weeks of age) and adult (12–14 weeks of age)

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Bajaj, Harpreet S., Chang Ye, Anthony J. Hanley, Mathew Sermer, Bernard Zinman, and Ravi Retnakaran. "Biomarkers of vascular injury and endothelial dysfunction after recent glucose intolerance in pregnancy." Diabetes and Vascular Disease Research 15, no. 5 (2018): 449–57. http://dx.doi.org/10.1177/1479164118779924.

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Objective: Women with gestational diabetes mellitus and milder gestational impaired glucose intolerance have elevated future risks of type 2 diabetes and cardiovascular disease. However, it is unclear whether they show postpartum evidence of vascular injury/dysfunction, an early event in the natural history of cardiovascular disease. Methods: In total, 337 women underwent a glucose challenge test and oral glucose tolerance test in pregnancy, yielding four gestational glucose tolerance groups: gestational diabetes mellitus, gestational impaired glucose intolerance, abnormal glucose challenge te

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Rigalleau, V., M. Beylot, C. Pachiaudi, C. Guillot, G. Deleris, and H. Gin. "Mechanisms of glucose intolerance during triglyceride infusion." American Journal of Physiology-Endocrinology and Metabolism 275, no. 4 (1998): E641—E648. http://dx.doi.org/10.1152/ajpendo.1998.275.4.e641.

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Lipid infusions may affect glucose tolerance by effects on glucose production or utilization. We performed double-labeled oral glucose tolerance tests with and without a lipid infusion in eight normal subjects. During the lipid infusion, plasma glucose and insulin levels were higher, showing some insulin resistance. The increased glucose level was due to a higher total glucose appearance rate, partly reproducible by a control infusion of glycerol [saline 1,181 ± 71 mg ⋅ kg−1 ⋅ 330 min−1 vs. lipid 1,388 ± 100 ( P < 0.05) vs. glycerol 1,276 ± 126 (NS)]. The tracer-determined appearance rate o

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Tonoike, Mie, Miyako Kishimoto, Mayumi Yamamoto, Tetsu Yano, and Mitsuhiko Noda. "Continuous Glucose Monitoring in Patients with Abnormal Glucose Tolerance during Pregnancy: A Case Series." Japanese Clinical Medicine 7 (January 2016): JCM.S34825. http://dx.doi.org/10.4137/jcm.s34825.

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Abnormal glucose tolerance during pregnancy is associated with perinatal complications. We used continuous glucose monitoring (CGM) in pregnant women with glucose intolerance to achieve better glycemic control and to evaluate the maternal glucose fluctuations. We also used CGM in women without glucose intolerance (the control cases). Furthermore, the standard deviation (SD) and mean amplitude of glycemic excursions (MAGE) were calculated for each case. For the control cases, the glucose levels were tightly controlled within a very narrow range; however, the SD and MAGE values in pregnant women

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6

Husseini, A. "Prevalence of diabetes mellitus and impaired glucose tolerance in a rural Palestinian population." Eastern Mediterranean Health Journal 6, no. 5-6 (2000): 1039–45. http://dx.doi.org/10.26719/2000.6.5-6.1039.

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The prevalence of diabetes mellitus and impaired glucose tolerance was investigated in a cross-sectional population-based study in a rural Palestinian population of 500 females and males aged 30-65 years. The prevalence of diabetes was 9.6% and 10.0% in females and males respectively. The prevalence of impaired glucose tolerance was 8.6%; 10.3% in females, 6.2% in males. The prevalence of total glucose intolerance [diabetes mellitus + impaired glucose tolerance]was 18.4%. Our study provides the first baseline data on diabetes mellitus and impaired glucose tolerance in Palestine. The results in

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7

Çapoğlu, I., N. Ünüvar, Y. Bektaş, Ö. Yilmaz, and MD Kaya. "The Effects of High Haematocrit Levels on Glucose Metabolism Disorders." Journal of International Medical Research 30, no. 4 (2002): 433–37. http://dx.doi.org/10.1177/147323000203000411.

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There has been only limited research investigating the possible association between raised haematocrit levels, glucose intolerance and type 2 diabetes. In the present study, we explored the association between high haematocrit levels and impaired glucose tolerance by performing oral glucose tolerance tests in 46 patients with chronic obstructive pulmonary disease and no previous history of diabetes mellitus or glucose intolerance. A glucose metabolism disorder was observed in 12 (26%) patients (type 2 diabetes in six patients and impaired glucose tolerance in a further six). There was a signif

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8

Mladenovic, Violeta, Milica Dimitrijevic-Stojanovic, Djuro Macut, and Aleksandar Djukic. "Glycoregulation During Pregnancy." Serbian Journal of Experimental and Clinical Research 20, no. 2 (2019): 9–16. http://dx.doi.org/10.1515/sjecr-2017-0009.

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Abstract Pregnancy is a period marked by profound changes in a woman’s hormonal status and metabolism, including the development of a carbohydrate-intolerant state. Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. The aim of this study was to estimate and analyse the parameters of glycaemic control during pregnancy. We stratified patients into the following three groups according to OGTT results: normal glucose tolerance (NTG), gestational impaired glucose tolerance (GIGT) and GDM. We investigated 92 pregnant

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9

Andrikopoulos, Sofianos, Amy R. Blair, Nadia Deluca, Barbara C. Fam, and Joseph Proietto. "Evaluating the glucose tolerance test in mice." American Journal of Physiology-Endocrinology and Metabolism 295, no. 6 (2008): E1323—E1332. http://dx.doi.org/10.1152/ajpendo.90617.2008.

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The objective of this study was to determine the optimal conditions under which to assess glucose tolerance in chow- and high-fat-fed C57BL/6J mice. Mice were fed either chow or high-fat diet for 8 wk. Variables tested were fasting duration (0-, 3-, 6-, and 24-h and overnight fasting), route of administration (intraperitoneal vs. oral) load of glucose given (2, 1, or 0.5 g/kg and fixed 50-mg dose), and state of consciousness. Basal glucose concentrations were increased in high-fat- compared with chow-fed mice following 6 h of fasting (9.1 ± 0.3 vs. 7.9 ± 0.4 mmol/l P = 0.01). Glucose tolerance

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10

Battram, D. S., J. Bugaresti, J. Gusba, and T. E. Graham. "Acute caffeine ingestion does not impair glucose tolerance in persons with tetraplegia." Journal of Applied Physiology 102, no. 1 (2007): 374–81. http://dx.doi.org/10.1152/japplphysiol.00901.2006.

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Acute caffeine (Caf) ingestion impairs glucose tolerance in able-bodied humans during an oral glucose tolerance test (OGTT). The mechanism responsible for this effect remains unclear, however, it is suggested to be due to the accompanying increase in epinephrine concentration. We examined whether or not Caf would elicit a glucose intolerance in persons with tetraplegia (TP) who do not exhibit an increased epinephrine response following Caf ingestion. All TP [ n = 14; 9 incomplete (Inc) lesion, 5 complete (Com) lesion] completed two OGTT 1 h after consuming either gelatin (Pl) or Caf capsules (

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Greco, A. V., L. Altomonte, G. Ghirlanda, et al. "Glucagon and glucose tolerance in liver cirrhosis." Acta Endocrinologica 118, no. 3 (1988): 337–45. http://dx.doi.org/10.1530/acta.0.1180337.

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Abstract. The present study was undertaken in order to establish the significance of glucagon in glucose intolerance in liver cirrhosis. The plasma glucose response to an oral glucose load (75 g) was determined in 10 control subjects and in 10 cirrhotic patients, after infusions of: glucagon (3 ng·kg−1·min−1) or saline (154 mmol/l); somatostatin (SRIH) (500 μg/h); and SRIH plus glucagon (3 ng·kg−1·min−1). Glucagon infusion did not impair glucose tolerance, neither in normal subjects nor in patients with cirrhosis. On the other hand, in both groups glucose tolerance was impaired by SRIH infusio

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12

Shimada, Hisao, Junji Uchida, Shunji Nishide, et al. "Comparison of Glucose Tolerance between Kidney Transplant Recipients and Healthy Controls." Journal of Clinical Medicine 8, no. 7 (2019): 920. http://dx.doi.org/10.3390/jcm8070920.

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Post-transplant hyperglycemia and new-onset diabetes mellitus after transplantation (NODAT) are common and important metabolic complications. Decreased insulin secretion and increased insulin resistance are important to the pathophysiologic mechanism behind NODAT. However, the progression of glucose intolerance diagnosed late after kidney transplantation remains clearly unknown. Enrolled in this study were 94 kidney transplant recipients and 134 kidney transplant donors, as the healthy controls, who were treated at our institution. The 75 g-oral glucose tolerance test (OGTT) was performed in t

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Muche, Achenef Asmamaw, Oladapo O. Olayemi, and Yigzaw Kebede Gete. "Predictors of postpartum glucose intolerance in women with gestational diabetes mellitus: a prospective cohort study in Ethiopia based on the updated diagnostic criteria." BMJ Open 10, no. 8 (2020): e036882. http://dx.doi.org/10.1136/bmjopen-2020-036882.

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ObjectivesTo identify the incidence of postpartum glucose intolerance and develop a prediction model based on antenatal characteristics to predict postpartum glucose intolerance.DesignProspective cohort study.SettingGondar town public health facilities in Northwest Ethiopia.ParticipantsWomen who had gestational diabetes mellitus were advised to undergo postpartum oral glucose tolerance test at 6–12 weeks of delivery.Main outcomePostpartum glucose intolerance.Data analysisPredictors of postpartum glucose intolerance were identified using multivariable logistic regression analysis. The discrimin

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14

Thomas, G. Neil, C. Mary Schooling, Sarah M. McGhee, et al. "Identification of factors differentially associated with isolated impaired fasting glucose and isolated post-load impaired glucose tolerance: the Hong Kong Cardiovascular Risk Factor Study." European Journal of Endocrinology 155, no. 4 (2006): 623–32. http://dx.doi.org/10.1530/eje.1.02250.

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Background: The use of fasting and post-prandial glucose levels in the classification of hyperglycaemic states often identifies distinct subjects, but the factors determining these intermediate-isolated glucose intolerant states are yet to be clearly elucidated in Chinese subjects. Methods: Representative subjects (n = 2769) were randomly recruited from the Hong Kong Chinese population and glycaemic status was determined using both fasting and 2h 75 g oral glucose tolerance test glucose levels. The relationship between the groups with isolated glucose intolerance and vascular risk factors was

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15

Kuk, Jennifer L., and Ruth E. Brown. "Aspartame intake is associated with greater glucose intolerance in individuals with obesity." Applied Physiology, Nutrition, and Metabolism 41, no. 7 (2016): 795–98. http://dx.doi.org/10.1139/apnm-2015-0675.

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This study examined whether sucrose, fructose, aspartame, and saccharin influences the association between obesity and glucose tolerance in 2856 adults from the NHANES III survey. Aspartame intake significantly influenced the association between body mass index (BMI) and glucose tolerance (interaction: P = 0.004), wherein only those reporting aspartame intake had a steeper positive association between BMI and glucose tolerance than those reporting no aspartame intake. Therefore, consumption of aspartame is associated with greater obesity-related impairments in glucose tolerance.

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16

Schaffer, S. W., B. H. Tan, and G. L. Wilson. "Development of a cardiomyopathy in a model of noninsulin-dependent diabetes." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 2 (1985): H179—H185. http://dx.doi.org/10.1152/ajpheart.1985.248.2.h179.

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Wistar rats were injected with streptozotocin (SZ) at 3 days of age. This maneuver produced a marked glucose intolerance, as determined by intraperitoneal glucose tolerance tests, but plasma fasting and nonfasting glucose values remained at or near normal throughout the 12-mo study period. Hearts obtained from these glucose-intolerant rats exhibited a progressive cardiomyopathy that consisted of both contractile and metabolic abnormalities. Contractile abnormalities were characterized by reductions in aortic output, ventricular pressure, and cardiac work. Associated with these mechanical defec

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17

Holness, M. J., and M. C. Sugden. "Continued glucose output after re-feeding contributes to glucose intolerance in hyperthyroidism." Biochemical Journal 247, no. 3 (1987): 801–4. http://dx.doi.org/10.1042/bj2470801.

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The effects of hyperthyroidism to elicit glucose intolerance after glucose administration were decreased under conditions where hepatic glucose output was suppressed. It is concluded that continued hepatic glucose output contributes to abnormal glucose tolerance in hyperthyroidism.

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18

Aouadi, Myriam, Pranitha Vangala, Joseph C. Yawe, et al. "Lipid storage by adipose tissue macrophages regulates systemic glucose tolerance." American Journal of Physiology-Endocrinology and Metabolism 307, no. 4 (2014): E374—E383. http://dx.doi.org/10.1152/ajpendo.00187.2014.

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Proinflammatory pathways in adipose tissue macrophages (ATMs) can impair glucose tolerance in obesity, but ATMs may also be beneficial as repositories for excess lipid that adipocytes are unable to store. To test this hypothesis, we selectively targeted visceral ATMs in obese mice with siRNA against lipoprotein lipase (LPL), leaving macrophages within other organs unaffected. Selective silencing of ATM LPL decreased foam cell formation in visceral adipose tissue of obese mice, consistent with a reduced supply of fatty acids from VLDL hydrolysis. Unexpectedly, silencing LPL also decreased the e

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Wogensen, Lise, Jesper Reimers, Thomas Mandrup-Poulsen та Jørn Nerup. "Repeated intraperitoneal injections of interleukin 1β induce glucose intolerance in normal rats". Acta Endocrinologica 124, № 5 (1991): 470–78. http://dx.doi.org/10.1530/acta.0.1240470.

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Abstract. Previous in vitro findings suggest the involvement of interleukin 1 (IL-1) in the pathogenesis of insulin-dependent diabetes mellitus. The aims of the present study were to investigate the effects of single or repeated ip injections of recombinant IL-1β on blood glucose and glucose tolerance in vivo. Normal Wistar Kyoto rats were injected ip with a single injection of 4 μg/kg of the mature form of recombinant IL-1β (amino acids 117-269) or once daily on 5 consecutive days. Control rats were given vehicle and were fed ad libitum or pair-fed together with the rIL-1β treated rats. An ip

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20

Phan, Thi To Nhu, and Trung Vinh Hoang. "Investigation of the progress in the women with gestational diabetes mellitus postpartum." Vietnam Journal of Diabetes and Endocrinology, no. 40 (January 28, 2021): 45–51. http://dx.doi.org/10.47122/vjde.2020.40.8.

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Aims: Our aim was to evaluate the uptake of postpartum screening, the prevalence and the risk factors for glucose intolerance in women with a recent history of gestational diabetes mellitus (GDM). Methods: All women with a history of GDM are advised to undergo a 75g oral glucose tolerance test (OGTT) around 6 - 12 weeks postpartum. Indices of insulin sensitivity (the Matsuda index and the reciprocal of the homeostasis model assessment of insulin resistance, HOMA-IR) and an index of beta-cell function, the Insulin Secretion-Sensitivity Index-2 (ISSI-2) were calculated based on the OGTT postpart

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Anderson, Eoin, Dan Cervone, and David James Dyck. "Late introduction of low dose resveratrol and grape powder after estradiol depletion does not restore glucose tolerance in the ovariectomized rat." Functional Foods in Health and Disease 8, no. 2 (2018): 79. http://dx.doi.org/10.31989/ffhd.v8i2.405.

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Background: Estrogen (E2) loss is associated with insulin resistance. Natural compounds such as resveratrol (RESV) have potential insulin sensitizing effects. Grape pomace powder (GP) also contains RESV and other antioxidants. However, the ability of realistic, attainable concentrations of RESV and GP to reverse glucose intolerance in E2 deficient rats has not yet been explored.Purpose: The aim of the current study was to determine whether RESV and GP, in realistic amounts that could be achieved with supplementation, would be effective in restoring glucose tolerance in the ovariectomized (OVX)

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Schindler, Christine E., Uttara Partap, Bonnie K. Patchen, and Steven J. Swoap. "Chronic rapamycin treatment causes diabetes in male mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 4 (2014): R434—R443. http://dx.doi.org/10.1152/ajpregu.00123.2014.

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Current evidence indicates that the mammalian target of rapamycin inhibitor rapamycin both increases longevity and, seemingly contradictorily, impairs glucose homeostasis. Most studies exploring the dimensions of this paradox have been based on rapamycin treatment in mice for up to 20 wk. We sought to better understand the metabolic effects of oral rapamycin over a substantially longer period of time in HET3 mice. We observed that treatment with rapamycin for 52 wk induced diabetes in male mice, characterized by hyperglycemia, significant urine glucose levels, and severe glucose and pyruvate i

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Jun, Jonathan C., Mi-Kyung Shin, Ronald Devera та ін. "Intermittent hypoxia-induced glucose intolerance is abolished by α-adrenergic blockade or adrenal medullectomy". American Journal of Physiology-Endocrinology and Metabolism 307, № 11 (2014): E1073—E1083. http://dx.doi.org/10.1152/ajpendo.00373.2014.

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Obstructive sleep apnea causes intermittent hypoxia (IH) during sleep and is associated with dysregulation of glucose metabolism. We developed a novel model of clinically realistic IH in mice to test the hypothesis that IH causes hyperglycemia, glucose intolerance, and insulin resistance via activation of the sympathetic nervous system. Mice were exposed to acute hypoxia of graded severity (21, 14, 10, and 7% O2) or to IH of graded frequency [oxygen desaturation index (ODI) of 0, 15, 30, or 60, SpO2nadir 80%] for 30 min to measure levels of glucose fatty acids, glycerol, insulin, and lactate.

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Kim, Sun-Young, Minsun Kim, Youngman Oh, and Dae-Yeol Lee. "Relationship of Serum Total Insulin-Like Growth Factor Binding Protein-3 with Insulin-Like Growth Factor-I and Glucose Tolerance in Korean Children and Adolescents." International Journal of Endocrinology 2021 (June 22, 2021): 1–8. http://dx.doi.org/10.1155/2021/9966114.

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Insulin is important in glucose metabolism. However, insulin-like growth factor binding protein (IGFBP) also plays an important role in glucose homeostasis, although the IGF-independent role of IGFBP-3 in the glucose intolerance state is poorly understood. We investigated the relationship of serum IGF-I with total IGFBP-3 levels and glucose tolerance in Korean children and adolescents who underwent the oral glucose tolerance test (OGTT). A total of 187 children without known diabetes underwent OGTT, and data related to their clinical and laboratory parameters were collected. Serum IGF-I and to

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Frangioudakis, G., J. Garrard, K. Raddatz, J. L. Nadler, T. W. Mitchell, and C. Schmitz-Peiffer. "Saturated- and n-6 Polyunsaturated-Fat Diets Each Induce Ceramide Accumulation in Mouse Skeletal Muscle: Reversal and Improvement of Glucose Tolerance by Lipid Metabolism Inhibitors." Endocrinology 151, no. 9 (2010): 4187–96. http://dx.doi.org/10.1210/en.2010-0250.

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Lipid-induced insulin resistance is associated with intracellular accumulation of inhibitory intermediates depending on the prevalent fatty acid (FA) species. In cultured myotubes, ceramide and phosphatidic acid (PA) mediate the effects of the saturated FA palmitate and the unsaturated FA linoleate, respectively. We hypothesized that myriocin (MYR), an inhibitor of de novo ceramide synthesis, would protect against glucose intolerance in saturated fat-fed mice, while lisofylline (LSF), a functional inhibitor of PA synthesis, would protect unsaturated fat-fed mice. Mice were fed diets enriched i

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Tominaga, Masato, Tadasu Ikeda, and Hiroto Mashiba. "Changes in urinary during oral glucose tolerance testing in patients with glucose intolerance." Clinica Chimica Acta 161, no. 3 (1986): 355–56. http://dx.doi.org/10.1016/0009-8981(86)90022-7.

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Lee, Jean C. "Altered Glucose Metabolism in HIV-infected Patients Treated With HAART." Journal of Pharmacy Practice 17, no. 1 (2004): 80–86. http://dx.doi.org/10.1177/0897190003261313.

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The introduction of protease inhibitors (PIs) has revolutionized the treatment of human immunodeficiency virus (HIV)– positive patients. The consequences of potential long-term metabolic complications have led to the use of PI-sparing regimens. As HIV treatment with PIs is associated with lipodystrophy (fat redistribution, hyperlipidemia, and glucose intolerance), it is essential to effectively manage these long-term toxicities. The impact of PI-induced glucose intolerance has resulted in studies investigating both pathogenesis andmanagement of this side effect. The action of PIs on the glucos

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Caillaud, Corinne, Mie Mechta, Heidi Ainge, et al. "Chronic erythropoietin treatment improves diet-induced glucose intolerance in rats." Journal of Endocrinology 225, no. 2 (2015): 77–88. http://dx.doi.org/10.1530/joe-15-0010.

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Erythropoietin (EPO) ameliorates glucose metabolism through mechanisms not fully understood. In this study, we investigated the effect of EPO on glucose metabolism and insulin signaling in skeletal muscle. A 2-week EPO treatment of rats fed with a high-fat diet (HFD) improved fasting glucose levels and glucose tolerance, without altering total body weight or retroperitoneal fat mass. Concomitantly, EPO partially rescued insulin-stimulated AKT activation, reduced markers of oxidative stress, and restored heat-shock protein 72 expression in soleus muscles from HFD-fed rats. Incubation of skeleta

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Benhalima, Katrien, Paul Van Crombrugge, Carolien Moyson, et al. "Prediction of Glucose Intolerance in Early Postpartum in Women with Gestational Diabetes Mellitus Based on the 2013 WHO Criteria." Journal of Clinical Medicine 8, no. 3 (2019): 383. http://dx.doi.org/10.3390/jcm8030383.

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Predictors for glucose intolerance postpartum were evaluated in women with gestational diabetes mellitus (GDM) based on the 2013 World Health Organization (WHO) criteria. 1841 women were tested for GDM in a prospective cohort study. A postpartum 75g oral glucose tolerance test (OGTT) was performed in women with GDM at 14 ± 4.1 weeks. Of all 231 mothers with GDM, 83.1% (192) had a postpartum OGTT of which 18.2% (35) had glucose intolerance. Women with glucose intolerance were more often of Asian origin [15.1% vs. 3.7%, OR 4.64 (1.26–17.12)], had more often a recurrent history of GDM [41.7% vs.

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Parlevliet, Edwin T., Annemieke C. Heijboer, Janny P. Schröder-van der Elst, et al. "Oxyntomodulin ameliorates glucose intolerance in mice fed a high-fat diet." American Journal of Physiology-Endocrinology and Metabolism 294, no. 1 (2008): E142—E147. http://dx.doi.org/10.1152/ajpendo.00576.2007.

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We evaluated the acute effects of OXM on glucose metabolism in diet-induced insulin-resistant male C57Bl/6 mice. To determine the effects on glucose tolerance, mice were intraperitoneally injected with OXM (0.75, 2.5, or 7.5 nmol) or vehicle prior to an ip glucose tolerance test. OXM (0.75 nmol/h) or vehicle was infused during a hyperinsulinemic euglycemic clamp to quantify insulin action on glucose production and disposal. OXM dose-dependently improved glucose tolerance as estimated by AUC for glucose (OXM: 7.5 nmol, 1,564 ± 460, P < 0.01; 2.5 nmol, 1,828 ± 684, P < 0.01; 0.75 nmol, 2,3

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Zorrón Mei Hsia Pu, Mariana, Aline Cristina Gonçalves, Walter José Minnicucci, André Moreno Morcillo, José Dirceu Ribeiro, and Antonio Fernando Ribeiro. "Continuous glucose monitoring to evaluate glycaemic abnormalities in cystic fibrosis." Archives of Disease in Childhood 103, no. 6 (2018): 592–96. http://dx.doi.org/10.1136/archdischild-2017-314250.

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ObjectiveThis study aimed to determine the glycaemic profile of patients with cystic fibrosis using a continuous glucose monitoring system (CGMS), and to evaluate the associations of glycaemic abnormalities with sex, age, pubertal stage, CFTR gene mutations, nutritional status, lung function, oral glucose tolerance test, glycated haemoglobin concentrations, fasting insulin concentrations, C peptide concentrations and exocrine pancreatic function.Study designThis observational study evaluated CGMS data from 39 patients with cystic fibrosis who were treated at a referral centre. The patients wer

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Gari, Manju, Abhishek Kumar, and Lakhan Majhee. "Effect of atorvastatin and rosuvastatin on glucose intolerance in low dose streptozotocin induced hyperglycemic Albino rats." International Journal of Basic & Clinical Pharmacology 6, no. 7 (2017): 1747. http://dx.doi.org/10.18203/2319-2003.ijbcp20172742.

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Background: Dyslipidemia and glucose intolerance are closely associated with each other especially as a part of metabolic syndrome. Statins are the drug of choice for treatment of dyslipidemia and for primary prevention of coronary heart disease in diabetics. Recent studies indicate risk of new onset diabetes in patients receiving statins. Hence it was worthwhile to study the effect of two most commonly used statins, which differ in their lipophilicity, on glucose tolerance in prediabetic animal model.Methods: The study consisted of 3 groups with 6 wistar rats in each and hyperglycemia was ind

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Varillas, Dora, and VF Varillas. "Early glucose intolerance postpartum of gestational diabetes associated with overload test with 50 grams of glucose." Problems of Endocrinology 62, no. 5 (2016): 30–31. http://dx.doi.org/10.14341/probl201662530-31.

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Introduction. The glucose intolerance later gestational diabetes is a very important indicator that helps establish the prognosis of diabetes in pregnant women who have had gestational diabetes (1). In this study we followed for one year to all gestational diabetes who were treated at the Hospital of Fuerteventura in endocrinology consultation,Canary Island, Spain. The aim was to study what factors might be related to glucose intolerance in the immediate postpartum.Materials and methods. All pregnant women served with the diagnosis of gestational diabetes during April 2012 to May 2013, diagnos

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ASHINO, Yoshikazu, Yasuo OWADA, Kioaki OUCHI, and Ryuji SATO. "The quantitative assessment of the glucose intolerance in cirrhosis by intravenous glucose tolerance test and insulin tolerance test." Kanzo 28, no. 8 (1987): 1057–64. http://dx.doi.org/10.2957/kanzo.28.1057.

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Williams, Deon B., Zhongxiao Wan, Bruce C. Frier, Rhonda C. Bell, Catherine J. Field, and David C. Wright. "Dietary supplementation with vitamin E and C attenuates dexamethasone-induced glucose intolerance in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 1 (2012): R49—R58. http://dx.doi.org/10.1152/ajpregu.00304.2011.

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Glucocorticoid excess induces marked insulin resistance and glucose intolerance. A recent study has shown that antioxidants prevent dexamethasone (DEX)-induced insulin resistance in cultured adipocytes. The purpose of this investigation was to examine the effects of dietary vitamin E and C (Vit E/C) supplementation on DEX-induced glucose intolerance in rats. We hypothesized that feeding rats a diet supplemented with Vit E/C would improve glucose tolerance and restore insulin signaling in skeletal muscle, adipose, and liver and prevent alterations in AMPK signaling in these tissues. Male Wistar

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García-Tornadú, Isabel, Ana M. Ornstein, Astrid Chamson-Reig, et al. "Disruption of the Dopamine D2 Receptor Impairs Insulin Secretion and Causes Glucose Intolerance." Endocrinology 151, no. 4 (2010): 1441–50. http://dx.doi.org/10.1210/en.2009-0996.

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The relationship between antidopaminergic drugs and glucose has not been extensively studied, even though chronic neuroleptic treatment causes hyperinsulinemia in normal subjects or is associated with diabetes in psychiatric patients. We sought to evaluate dopamine D2 receptor (D2R) participation in pancreatic function. Glucose homeostasis was studied in D2R knockout mice (Drd2−/−) mice and in isolated islets from wild-type and Drd2−/− mice, using different pharmacological tools. Pancreas immunohistochemistry was performed. Drd2−/− male mice exhibited an impairment of insulin response to gluco

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Brewster, Shireen, John Floras, Bernard Zinman, and Ravi Retnakaran. "Endothelial Function in Women with and without a History of Glucose Intolerance in Pregnancy." Journal of Diabetes Research 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/382670.

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Background/Aims. Gestational diabetes mellitus (GDM) and milder gestational impaired glucose tolerance (GIGT) identify women who are at risk of developing cardiovascular disease. Endothelial dysfunction, as indicated by impaired flow-mediated dilatation (FMD) on brachial artery ultrasound, is an early marker of vascular disease. Thus, we sought to evaluate endothelial function in women with and without recent glucose intolerance in pregnancy.Methods. One-hundred and seventeen women underwent oral glucose tolerance testing (OGTT) in pregnancy, enabling stratification into those with normal gest

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Bhattacharyya, Sumit, Leo Feferman, Terry Unterman, and Joanne K. Tobacman. "Exposure to Common Food Additive Carrageenan Alone Leads to Fasting Hyperglycemia and in Combination with High Fat Diet Exacerbates Glucose Intolerance and Hyperlipidemia without Effect on Weight." Journal of Diabetes Research 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/513429.

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Aims. Major aims were to determine whether exposure to the commonly used food additive carrageenan could induce fasting hyperglycemia and could increase the effects of a high fat diet on glucose intolerance and dyslipidemia.Methods. C57BL/6J mice were exposed to either carrageenan, high fat diet, or the combination of high fat diet and carrageenan, or untreated, for one year. Effects on fasting blood glucose, glucose tolerance, lipid parameters, weight, glycogen stores, and inflammation were compared.Results. Exposure to carrageenan led to glucose intolerance by six days and produced elevated

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Ziemer, David C., Paul Kolm, Jovonne K. Foster, et al. "Random Plasma Glucose in Serendipitous Screening for Glucose Intolerance: Screening for Impaired Glucose Tolerance Study 2." Journal of General Internal Medicine 23, no. 5 (2008): 528–35. http://dx.doi.org/10.1007/s11606-008-0524-1.

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Sakaguchi, Kazuhiko, Kazuo Takeda, Mitsuo Maeda, et al. "Glucose area under the curve during oral glucose tolerance test as an index of glucose intolerance." Diabetology International 7, no. 1 (2015): 53–58. http://dx.doi.org/10.1007/s13340-015-0212-4.

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Corrado, F., R. D’Anna, A. S. Laganà, and A. Di Benedetto. "Abnormal glucose tolerance later in life in women affected by glucose intolerance during pregnancy." Journal of Obstetrics and Gynaecology 34, no. 2 (2014): 123–26. http://dx.doi.org/10.3109/01443615.2013.841658.

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Festuccia, William T., Pierre-Gilles Blanchard, Thiago Belchior та ін. "PPARγ activation attenuates glucose intolerance induced by mTOR inhibition with rapamycin in rats". American Journal of Physiology-Endocrinology and Metabolism 306, № 9 (2014): E1046—E1054. http://dx.doi.org/10.1152/ajpendo.00683.2013.

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mTOR inhibition with rapamycin induces a diabetes-like syndrome characterized by severe glucose intolerance, hyperinsulinemia, and hypertriglyceridemia, which is due to increased hepatic glucose production as well as reduced skeletal muscle glucose uptake and adipose tissue PPARγ activity. Herein, we tested the hypothesis that pharmacological PPARγ activation attenuates the diabetes-like syndrome associated with chronic mTOR inhibition. Rats treated with the mTOR inhibitor rapamycin (2 mg·kg−1·day−1) in combination or not with the PPARγ ligand rosiglitazone (15 mg·kg−1·day−1) for 15 days were

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K.C., Kamana, Hua Zhang, and Anju Vaidya. "Increased Incidence in False Positive Diagnosis of Gestational Diabetes Mellitus with 75gm Oral Glucose Tolerance Test: A Clinical Study in Chinese Women." Journal of Nepal Health Research Council 17, no. 01 (2019): 103–8. http://dx.doi.org/10.33314/jnhrc.v17i01.1588.

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Background: Currently, most of the countries across the globe follow the International Association of the Diabetes and Pregnancy Study Groups criteria in the diagnosis of gestational diabetes mellitus, which is based on the analysis of Hyperglycemia and Adverse Pregnancy Outcome study. The International Association of the Diabetes and Pregnancy Study Groups criterion comes with its benefits and doubts. Although it has been adopted worldwide, diagnosis of gestational diabetes mellitus with single test and only one positive value has always been debated and is often criticized. This study aimed

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Zhang, Bingjie, Jing Wang, Shanmei Shen, et al. "Association of Androgen Excess with Glucose Intolerance in Women with Polycystic Ovary Syndrome." BioMed Research International 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/6869705.

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Women with polycystic ovary syndrome (PCOS) show high prevalence of glucose intolerance. This study aimed to investigate the association of androgen excess with glucose intolerance in PCOS. A total of 378 women with PCOS participated in the study. Free androgen index (FAI) was selected as indicator of hyperandrogenism. Insulin sensitivity was assessed by 1/homeostasis model assessment of insulin resistance (1/HOMA-IR) and Matsuda insulin sensitivity index (ISIM); β-cell function was assessed by disposition index (DI). We found that women with glucose intolerance had higher FAI levels compared

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Dimova, Rumyana, Tsvetalina Tankova, Georgi Kirilov, Nevena Chakarova, Greta Grozeva, and Lilia Dakovska. "Endothelial and Autonomic Dysfunction at Early Stages of Glucose Intolerance and in Metabolic Syndrome." Hormone and Metabolic Research 52, no. 01 (2019): 39–48. http://dx.doi.org/10.1055/a-0972-1302.

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AbstractThis study evaluated sE-selectin, Endothelin-1, and cardiovascular autonomic neuropathy (CAN) at early stages of glucose intolerance and in metabolic syndrome (MetS). A total of 87 subjects – 39 males, of mean age 45.7±11.6 years and mean BMI 31.4±6.6 kg/m2, divided according to glucose tolerance and the presence of MetS were enrolled. Glucose tolerance was studied during OGTT. Anthropometric indices, blood pressure, HbA1c, lipids, hsCRP, sE-selectin, Endothelin-1, and immunoreactive insulin were measured. Body composition was assessed by a bioimpedance method (InBody 720, BioSpace). T

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Legro, Richard S., Carol L. Gnatuk, Allen R. Kunselman, and Andrea Dunaif. "Changes in Glucose Tolerance over Time in Women with Polycystic Ovary Syndrome: A Controlled Study." Journal of Clinical Endocrinology & Metabolism 90, no. 6 (2005): 3236–42. http://dx.doi.org/10.1210/jc.2004-1843.

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We performed this study to access the changes in glucose tolerance over time in a group of women with polycystic ovary syndrome (PCOS) (n = 71) and control women (n = 23) with regular menstrual cycles and baseline normal glucose tolerance. Mean follow-up was between 2 and 3 yr for both groups (PCOS 2.5 ± 1.7 yr; controls 2.9 ± 2.1 yr). Based on World Health Organization glucose tolerance categories, there was no significant difference in the prevalence of glucose intolerance at follow-up in the PCOS group. In the PCOS group, 25 (37%) had impaired glucose tolerance (IGT) and seven (10%) had typ

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Ahrén, Bo, and Giovanni Pacini. "Impaired adaptation of first-phase insulin secretion in postmenopausal women with glucose intolerance." American Journal of Physiology-Endocrinology and Metabolism 273, no. 4 (1997): E701—E707. http://dx.doi.org/10.1152/ajpendo.1997.273.4.e701.

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This study examined whether insulin secretion, insulin sensitivity, glucose effectiveness, and hepatic extraction of insulin are altered in subjects with impaired glucose tolerance (IGT). The frequently sampled intravenous glucose tolerance test was performed in postmenopausal women (age 63 yr, body mass index range 21.6–28.9 kg/m2) with IGT ( n = 10) or normal glucose tolerance (NGT; n = 10). Insulin sensitivity (SI) was significantly lower in IGT than in NGT ( P = 0.030). In contrast, insulin secretion was not significantly different between the two groups as determined by area under the cur

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Blesson, Chellakkan S., Amy K. Schutt, Vidyadharan A. Vipin, et al. "In utero low-protein-diet-programmed type 2 diabetes in adult offspring is mediated by sex hormones in rats†." Biology of Reproduction 103, no. 5 (2020): 1110–20. http://dx.doi.org/10.1093/biolre/ioaa133.

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Abstract Sex steroids regulate insulin sensitivity and glucose metabolism. We had characterized a lean type 2 diabetes (T2D) rat model using gestational low-protein (LP) diet programming. Our objective was to identify if endocrine dysfunction leading to decreased sex hormone levels will precede the development of T2D and if steroid replacement will prevent the onset of the disease. Pregnant rats were fed control or isocaloric LP diet from gestational day 4 until delivery. Normal diet was given to all mothers after delivery and to pups after weaning. LP offspring developed glucose intolerance a

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Shinohara, Masami, Toshihiro Oikawa, Kahei Sato, and Yasunori Kanazawa. "Glucose Intolerance and Hyperlipidemia Prior to Diabetes Onset in Female Spontaneously Diabetic Torii (SDT) Rats." Experimental Diabesity Research 5, no. 4 (2004): 253–56. http://dx.doi.org/10.1080/15438600490898609.

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The Spontaneously Diabetic Torii (SDT) rat, a newly established animal model for diabetes mellitus, presents nonobese type 2 diabetes with ocular complications. In the present study, oral glucose tolerance tests and biochemical and histopathological examinations were performed in female SDT rats at 16 and/or 25 weeks of age, before the onset of diabetes. At 25 weeks of age, glucose tolerance was significantly impaired, and plasma immunoreactive insulin levels at 120 min after glucose loading were significantly higher (P< 0.05). Body weight and fasting levels of plasma triglycerides and none

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Sharma, Nirmala, and Durga BC. "Screening of Diabetes in Pregnancy at Nepalgunj Medical College Teaching Hospital Kohalpur." Journal of Nepalgunj Medical College 18, no. 2 (2021): 63–67. http://dx.doi.org/10.3126/jngmc.v18i2.38911.

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Introduction: Gestational Diabetes Mellitus (GDM) is defined as glucose intolerance of variable severity or hyperglycemia occuring for the first time during pregnancy but the glucose intolerance reverting back to normal after the puerperium. According to American Diabetic Association, approximately 7% of all pregnancy are complicated by Gestational Diabetes Mellitus, resulting in more than two lakhs cases annually and the prevalence may range from 1-14% of all pregnancies. Gestational Diabetes Mellitus usually develop in the second trimester and carries grave prognosis both for mother and fetu

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