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Artículos de revistas sobre el tema "Insulin metabolism"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 25 de julio de 2025

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1

Humaira, Thisa, and Rizka Sofia. "Pasien Diabetes Melitus dengan Penatalaksanaan Gigi Tiruan Penuh (GTP)." GALENICAL : Jurnal Kedokteran dan Kesehatan Mahasiswa Malikussaleh 3, no. 2 (2024): 115. http://dx.doi.org/10.29103/jkkmm.v3i2.17359.

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Diabetes mellitus (DM) didefinisikan sebagai suatu penyakit atau gangguan metabolisme kronis dengan multi etiologi yang ditandai dengan tingginya kadar gula darah disertai dengan gangguan metabolism karbohidrat, lipid dan protein sebagai akibat insufisiensi fungsi insuli. Insufisiensi fungsi insulin dapat di sebabkan oleh gangguan atau defisiensi produksi insulin oleh sel – sel beta Langerhans kelenjar beta pancreas atau disebabkan kurang responsifnya sel – sel tubuh terhadap insulin. Penyakit ini dapat menimbulkan banyak komplikasi di berbagai bagian tubuh, ternasuk rongga mulut. Beberapa man

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2

Ukkola, O. "Ghrelin and insulin metabolism." European Journal of Clinical Investigation 33, no. 3 (2003): 183–85. http://dx.doi.org/10.1046/j.1365-2362.2003.01112.x.

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3

Duckworth, William C., Frederick G. Hamel, and Daniel E. Peavy. "Hepatic metabolism of insulin." American Journal of Medicine 85, no. 5 (1988): 71–76. http://dx.doi.org/10.1016/0002-9343(88)90399-3.

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4

Heesom, K. J., M. Harbeck, C. R. Kahn, and R. M. Denton. "Insulin action on metabolism." Diabetologia 40 (September 19, 1997): S3—S9. http://dx.doi.org/10.1007/s001250051388.

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5

Beardsall, Kathryn, Barbro M. S. Diderholm, and David B. Dunger. "Insulin and carbohydrate metabolism." Best Practice & Research Clinical Endocrinology & Metabolism 22, no. 1 (2008): 41–55. http://dx.doi.org/10.1016/j.beem.2007.10.001.

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6

Heesom, K. J., M. Harbeck, C. R. Kahn, and R. M. Denton. "Insulin action on metabolism." Diabetologia 40, S3 (1997): B3—B9. http://dx.doi.org/10.1007/bf03168179.

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7

Harned, Leighton Kahle, and Edward Chin. "PSUN278 Factitious hypoglycemia, diagnostic delay due to insulin assay failure to detect insulin analogues." Journal of the Endocrine Society 6, Supplement_1 (2022): A403. http://dx.doi.org/10.1210/jendso/bvac150.838.

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Abstract Factitious hypoglycemia may be difficult to diagnose clinically. Hypoglycemia due to insulin self-administration is established by the presence of a low c-peptide and elevated plasma insulin levels. Commercial insulin assays often fail to detect insulin analogs and can create confusion among providers investigating causes of hypoglycemia. A 20 year old female with no significant past medical history presented to an Emergency Room (ER) with hypoglycemia. She was treated with a single dose of octreotide 150 mcg, dexamethasone 10 mg PO and started on a D10W drip at 100ml/hr prior to tran

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8

Hirsch, Irl B., Rattan Juneja, John M. Beals, Caryl J. Antalis, and Eugene E. Wright. "The Evolution of Insulin and How it Informs Therapy and Treatment Choices." Endocrine Reviews 41, no. 5 (2020): 733–55. http://dx.doi.org/10.1210/endrev/bnaa015.

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Abstract Insulin has been available for the treatment of diabetes for almost a century, and the variety of insulin choices today represents many years of discovery and innovation. Insulin has gone from poorly defined extracts of animal pancreata to pure and precisely controlled formulations that can be prescribed and administered with high accuracy and predictability of action. Modifications of the insulin formulation and of the insulin molecule itself have made it possible to approximate the natural endogenous insulin response. Insulin and insulin formulations had to be designed to produce ei

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9

Piloquet, H., V. Ferchaud-Roucher, F. Duengler, Y. Zair, P. Maugere, and M. Krempf. "Insulin effects on acetate metabolism." American Journal of Physiology-Endocrinology and Metabolism 285, no. 3 (2003): E561—E565. http://dx.doi.org/10.1152/ajpendo.00042.2003.

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Acetate metabolism was studied in patients with insulin resistance. To evaluate the interaction between glucose and acetate metabolism, we measured acetate and glucose turnover with a hyperinsulinemic euglycemic clamp (hot clamp) in obese and diabetic patients with insulin resistance ( n = 8) and in a control group with normal insulin sensitivity ( n = 6). At baseline, acetate turnover and plasma concentrations were similar between the two groups (group means: 4.3 ± 0.4 μmol · kg-1 · min-1 and 128.2 ± 11.1 μmol/l). Acetate concentrations decreased in both groups with hyperinsulinemia but were

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10

Wu, Xinyue. "Lipid metabolism and insulin sensitivity." Theoretical and Natural Science 46, no. 1 (2024): 23–29. http://dx.doi.org/10.54254/2753-8818/46/20240400.

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Diabetes mellitus is known to be a serious chronic disease that requires great attention because it is the cancer that never dies and affects many people worldwide; its later complications are often numerous and frightening, and some of them may even affect their children as hereditary diseases. The relationship between lipid metabolism and insulin sensitivity in relation to diabetes is therefore even more important in this context. Insulin plays an important role as a key metabolic hormone in regulating glucose intake and maintaining lipid metabolic homeostasis. Insulin resistance interferes

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11

TAKAHASHI, Shin-Ichirou. "Hormone and protein metabolism. Insulin and protein metabolism." Journal of the agricultural chemical society of Japan 61, no. 10 (1987): 1300–1304. http://dx.doi.org/10.1271/nogeikagaku1924.61.1300.

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12

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (2018): 01–02. http://dx.doi.org/10.31579/2640-1045/096.

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Our laboratory has investigated two hypotheses regarding the effects of fructose consumption: 1) The endocrine effects of fructose consumption favor a positive energy balance, and 2) Fructose consumption promotes the development of an atherogenic lipid profile. In previous short- and long-term studies, we demonstrated that consumption of fructose-sweetened beverages with 3 meals results in lower 24-hour plasma concentrations of glucose, insulin, and leptin in humans compared with consumption of glucose-sweetened beverages. We have also tested whether prolonged consumption of high-fructose diet

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13

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (2018): 01–02. http://dx.doi.org/10.31579/2640-1045/021.

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14

Khoshnejat, Maryam, Ali Mohammad Banaei-Moghaddam, Ali Akbar Moosavi-Movahedi, and Kaveh Kavousi. "A holistic view of muscle metabolic reprogramming through personalized metabolic modeling in newly diagnosed diabetic patients." PLOS ONE 18, no. 6 (2023): e0287325. http://dx.doi.org/10.1371/journal.pone.0287325.

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Type 2 diabetes mellitus (T2DM) is a challenging and progressive metabolic disease caused by insulin resistance. Skeletal muscle is the major insulin-sensitive tissue that plays a pivotal role in blood sugar homeostasis. Dysfunction of muscle metabolism is implicated in the disturbance of glucose homeostasis, the development of insulin resistance, and T2DM. Understanding metabolism reprogramming in newly diagnosed patients provides opportunities for early diagnosis and treatment of T2DM as a challenging disease to manage. Here, we applied a system biology approach to investigate metabolic dysr

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15

Ikeoka, Dimas, and Eva Krusinova. "Insulin resistance and lipid metabolism." Revista da Associação Médica Brasileira 55, no. 3 (2009): 234. http://dx.doi.org/10.1590/s0104-42302009000300003.

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16

Blatniczky, L., L. Kautzky, and F. Péter. "Insulin Metabolism in Hypothalamic Obesity." Experimental and Clinical Endocrinology & Diabetes 96, no. 04 (2009): 83–89. http://dx.doi.org/10.1055/s-0029-1210992.

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17

Howard, Barbara V. "Insulin resistance and lipid metabolism." American Journal of Cardiology 84, no. 1 (1999): 28–32. http://dx.doi.org/10.1016/s0002-9149(99)00355-0.

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18

Biolo, Gianni, and Robert R. Wolfe. "Insulin action on protein metabolism." Baillière's Clinical Endocrinology and Metabolism 7, no. 4 (1993): 989–1005. http://dx.doi.org/10.1016/s0950-351x(05)80242-3.

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19

Frayn, Keith N. "Insulin resistance and lipid metabolism." Current Opinion in Lipidology 4, no. 3 (1993): 197–204. http://dx.doi.org/10.1097/00041433-199306000-00004.

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20

Taskinen, Marja-Riitta. "Insulin resistance and lipoprotein metabolism." Current Opinion in Lipidology 6, no. 3 (1995): 153–60. http://dx.doi.org/10.1097/00041433-199506000-00007.

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21

Langouche, Lies, and Greet Van den Berghe. "Glucose Metabolism and Insulin Therapy." Critical Care Clinics 22, no. 1 (2006): 119–29. http://dx.doi.org/10.1016/j.ccc.2005.09.005.

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22

York, Ashley. "Bacterial metabolism influences insulin resistance." Nature Reviews Microbiology 21, no. 11 (2023): 703. http://dx.doi.org/10.1038/s41579-023-00977-0.

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23

Del Prato, S., R. A. DeFronzo, P. Castellino, J. Wahren, and A. Alvestrand. "Regulation of amino acid metabolism by epinephrine." American Journal of Physiology-Endocrinology and Metabolism 258, no. 5 (1990): E878—E887. http://dx.doi.org/10.1152/ajpendo.1990.258.5.e878.

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The effect of epinephrine on amino acid (AA) metabolism was examined in 33 healthy volunteers who participated in four studies. Nine subjects participated in study I, which consisted of four parts: euglycemic insulin clamp, insulin plus epinephrine, insulin plus epinephrine plus propranolol, and insulin plus propranolol. In study II six subjects received epinephrine with hepatic-femoral venous catheterization. In study III five individuals received epinephrine with somatostatin plus basal insulin replacement. In study IV quadriceps muscle biopsy was performed in six subjects after epinephrine

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24

Gargiulo, P., U. Di Mario, O. Zuccarini, et al. "Treatment of diabetic pregnant women with monocomponent insulins." Acta Endocrinologica 113, no. 3_Suppl (1986): S60—S65. http://dx.doi.org/10.1530/acta.0.111s0060.

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Abstract. Very little immunological research has been undertaken in pregnant diabetic women in relation to insulin therapy. We investigated the relations between treatment with insulins of varied immunogenic character and the presence of immune factors such as insulin antibodies, immune complexes and insulin antiinsulin complexes as well as some maternal and neonatal complications of diabetic pregnancy. 128 insulin treated diabetic pregnant women and 121 of their newborns were included in the study. The incidence of insulin antibodies, immune complexes and insulin antiinsulin complexes was low

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25

Panovska, S. "Insulin Resistance Realationship To Glucose Metabolism And Insulin Levels." Clinical Nutrition ESPEN 54 (April 2023): 666. http://dx.doi.org/10.1016/j.clnesp.2022.09.609.

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26

Bonen, Arend, G. Lynis Dohm, and Luc J. C. van Loon. "Lipid metabolism, exercise and insulin action." Essays in Biochemistry 42 (November 27, 2006): 47–59. http://dx.doi.org/10.1042/bse0420047.

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Skeletal muscle constitutes 40% of body mass and takes up 80% of a glucose load. Therefore, impaired glucose removal from the circulation, such as that which occurs in obesity and type 2 diabetes, is attributable in large part to the insulin resistance in muscle. Recent research has shown that fatty acids, derived from adipose tissue, can interfere with insulin signalling in muscle. Hence, insulin-stimulated GLUT4 translocation to the cell surface is impaired, and therefore, the rate of glucose removal from the circulation into muscle is delayed. The mechanisms provoking lipid-mediated insulin

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27

Rossetti, L., G. Klein-Robbenhaar, G. Giebisch, D. Smith, and R. DeFronzo. "Effect of insulin on renal potassium metabolism." American Journal of Physiology-Renal Physiology 252, no. 1 (1987): F60—F64. http://dx.doi.org/10.1152/ajprenal.1987.252.1.f60.

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The effect of insulin on renal potassium excretion was examined by employing the euglycemic insulin clamp technique in combination with renal clearance measurements. While euglycemia was maintained, insulin was infused at rates of 4.8 (n = 7) and 12 (n = 5) mU X kg-1 X min-1. Steady-state plasma insulin levels of 164 +/- 8 and 370 +/- 15 microU/ml were achieved in the low- and high-dose studies, respectively. Base-line plasma potassium concentration declined progressively by a mean of 0.14 +/- 0.09 (P less than 0.05) and 0.40 +/- 0.05 meq/liter (P less than 0.01) during the low- and high-dose

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28

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 chromatog

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29

Thong, Farah S. L., and Terry E. Graham. "The Putative Roles of Adenosine in Insulin- and Exercise-Mediated Regulation of Glucose Transport and Glycogen Metabolism in Skeletal Muscle." Canadian Journal of Applied Physiology 27, no. 2 (2002): 152–78. http://dx.doi.org/10.1139/h02-011.

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Skeletal muscle is the primary site of whole-body glucose disposal and is vital in determining the overall insulin sensitivity and carbohydrate management. Insulin and physical exercise are important stimuli for muscle glucose transport and glycogen metabolism. While it is known that both insulin and contraction stimulate muscle glucose uptake and glycogen metabolism, the post-receptor mechanisms are not completely understood. Local metabolic factors, such as adenosine, have been suggested to play a role in insulin and contraction regulation of carbohydrate metabolism in skeletal muscle. While

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30

Demidova, Tatiana Y., and Olga V. Balutina. "Special aspects of concentrated insulins: basic characteristics and research findings." Diabetes mellitus 22, no. 5 (2020): 481–90. http://dx.doi.org/10.14341/dm10334.

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The appearance of concentrated insulins in clinical practice determines the need to analyze product priorities in appropriate groups of patients with diabetes. The aim of this article is to summarize the literature on concentrated insulins (i.e. insulin lispro 200 units/mL, insulin degludec 200 units/mL, insulin glargine 300 units/mL) from randomized controlled trials, derive guidance on appropriate and safe use of these agents and demonstrate experience in real clinical practice. Severe hypoglycemia in all studies was generally low (though higher with prandial plus concentrated basal analogue

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31

K Ivaska, Kaisa, Maikki K Heliövaara, Pertti Ebeling, et al. "The effects of acute hyperinsulinemia on bone metabolism." Endocrine Connections 4, no. 3 (2015): 155–62. http://dx.doi.org/10.1530/ec-15-0022.

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Insulin signaling in bone-forming osteoblasts stimulates bone formation and promotes the release of osteocalcin (OC) in mice. Only a few studies have assessed the direct effect of insulin on bone metabolism in humans. Here, we studied markers of bone metabolism in response to acute hyperinsulinemia in men and women. Thirty-three subjects from three separate cohorts (n=8, n=12 and n=13) participated in a euglycaemic hyperinsulinemic clamp study. Blood samples were collected before and at the end of infusions to determine the markers of bone formation (PINP, total OC, uncarboxylated form of OC (

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32

Huang, Wan, Anantha Metlakunta, Nikolas Dedousis, Heidi K. Ortmeyer, Maja Stefanovic-Racic, and Robert M. O'Doherty. "Leptin Augments the Acute Suppressive Effects of Insulin on Hepatic Very Low-Density Lipoprotein Production in Rats." Endocrinology 150, no. 5 (2009): 2169–74. http://dx.doi.org/10.1210/en.2008-1271.

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It is well established that leptin increases the sensitivity of carbohydrate metabolism to the effects of insulin. Leptin and insulin also have potent effects on lipid metabolism. However, the effects of leptin on the regulation of liver lipid metabolism by insulin have not been investigated. The current study addressed the effects of leptin on insulin-regulated hepatic very low-density lipoprotein (VLDL) metabolism in vivo in rats. A 90-min hyperinsulinemic/euglycemic clamp (4 mU/kg · min−1) reduced plasma VLDL triglyceride (TG) by about 50% (P &lt; 0.001 vs. saline control). Importantly,

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33

Caturano, Alfredo, Raffaele Galiero, Erica Vetrano, et al. "Insulin–Heart Axis: Bridging Physiology to Insulin Resistance." International Journal of Molecular Sciences 25, no. 15 (2024): 8369. http://dx.doi.org/10.3390/ijms25158369.

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Insulin signaling is vital for regulating cellular metabolism, growth, and survival pathways, particularly in tissues such as adipose, skeletal muscle, liver, and brain. Its role in the heart, however, is less well-explored. The heart, requiring significant ATP to fuel its contractile machinery, relies on insulin signaling to manage myocardial substrate supply and directly affect cardiac muscle metabolism. This review investigates the insulin–heart axis, focusing on insulin’s multifaceted influence on cardiac function, from metabolic regulation to the development of physiological cardiac hyper

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34

Yang, Xilin, Zezhang Tao, Zhanyong Zhu, Hua Liao, Yueqiang Zhao, and Huajun Fan. "MicroRNA-593-3p regulates insulin-promoted glucose consumption by targeting Slc38a1 and CLIP3." Journal of Molecular Endocrinology 57, no. 4 (2016): 211–22. http://dx.doi.org/10.1530/jme-16-0090.

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Insulin plays an important role in the regulation of glucose metabolism. However, the molecular mechanisms involved are not entirely clarified. In this context, we found that miR-593-3p negatively regulates insulin-regulated glucose metabolism in hepatocellular carcinoma HepG2 and Bel7402 cells. We then identified Slc38a1 and CLIP3 as novel targets of miR-593-3p. Further studies demonstrated that Slc38a1 and CLIP3 mediate insulin-regulated glucose metabolism. Interestingly, we also demonstrated that miR-593-3p expression was negatively associated with Slc38a1 and CLIP3 expression in insulin-tr

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35

Borelli, María I., Flavio Francini, and Juan José Gagliardino. "Autocrine regulation of glucose metabolism in pancreatic islets." American Journal of Physiology-Endocrinology and Metabolism 286, no. 1 (2004): E111—E115. http://dx.doi.org/10.1152/ajpendo.00161.2003.

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We evaluated the possible autocrine modulatory effect of insulin on glucose metabolism and glucose-induced insulin secretion in islets isolated from normal hamsters. We measured 14CO2 and 3H2O production from d-[U-14C]glucose and d-[5-3H]glucose, respectively, in islets incubated with 0.6, 3.3, 8.3, and 16.7 mM glucose alone or with 5 or 15 mU/ml insulin, anti-insulin guinea pig serum (1:500), 25 μM nifedipine, or 150 nM wortmannin. Insulin release was measured (radioimmunoassay) in islets incubated with 3.3 or 16.7 mM glucose with or without 75, 150, and 300 nM wortmannin. Insulin significant

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36

Moreno-Aliaga, M. J., M. M. Swarbrick, S. Lorente-Cebrián, K. L. Stanhope, P. J. Havel, and J. A. Martínez. "Sp1-mediated transcription is involved in the induction of leptin by insulin-stimulated glucose metabolism." Journal of Molecular Endocrinology 38, no. 5 (2007): 537–46. http://dx.doi.org/10.1677/jme-06-0034.

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We have previously demonstrated that insulin-stimulated glucose metabolism, and not insulin per se, mediates the effects of insulin to increase the transcriptional activity of the leptin promoter in adipocytes. Here, we sought to identify the specific cis-acting DNA elements required for the upregulation of leptin gene transcription in response to insulin-mediated glucose metabolism. To accomplish this, 3T3-L1 cells and primary rat adipocytes were transfected with a series of luciferase reporter genes containing portions of the mouse leptin promoter. Using this method, we identified an element

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37

Tao, Zhipeng, and Zhiyong Cheng. "Hormonal regulation of metabolism—recent lessons learned from insulin and estrogen." Clinical Science 137, no. 6 (2023): 415–34. http://dx.doi.org/10.1042/cs20210519.

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Abstract Hormonal signaling plays key roles in tissue and metabolic homeostasis. Accumulated evidence has revealed a great deal of insulin and estrogen signaling pathways and their interplays in the regulation of mitochondrial, cellular remodeling, and macronutrient metabolism. Insulin signaling regulates nutrient and mitochondrial metabolism by targeting the IRS-PI3K-Akt-FoxOs signaling cascade and PGC1α. Estrogen signaling fine-tunes protein turnover and mitochondrial metabolism through its receptors (ERα, ERβ, and GPER). Insulin and estrogen signaling converge on Sirt1, mTOR, and PI3K in th

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Campbell, P. J., M. G. Carlson, and N. Nurjhan. "Fat metabolism in human obesity." American Journal of Physiology-Endocrinology and Metabolism 266, no. 4 (1994): E600—E605. http://dx.doi.org/10.1152/ajpendo.1994.266.4.e600.

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Excessive fat turnover and oxidation might cause the insulin resistance of carbohydrate metabolism in obese humans. We studied the response of free fatty acid (FFA) metabolism in lean and obese volunteers to sequential insulin infusions of 4, 8, 25, and 400 mU.m-2.min-1. The insulin dose-response curves for suppression of FFA concentration, FFA turnover ([1-14C]palmitate), and lipolysis ([2H5]glycerol) were shifted to the right in the obese subjects (insulin concentrations that produced a half-maximal response, lean vs. obese: 103 +/- 21 vs. 273 +/- 41, 96 +/- 11 vs. 264 +/- 44, and 101 +/- 23

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Koh, Han-Chow E., Stephan van Vliet, Chao Cao, et al. "Effect of obstructive sleep apnea on glucose metabolism." European Journal of Endocrinology 186, no. 4 (2022): 457–67. http://dx.doi.org/10.1530/eje-21-1025.

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Background Obstructive sleep apnea (OSA) is prevalent in people with obesity and is a major risk factor for type 2 diabetes (T2D). The effect of OSA on metabolic function and the precise mechanisms (insulin resistance, β-cell dysfunction, or both) responsible for the increased T2D risk in people with OSA are unknown. Design and methods We used a two-stage hyperinsulinemic–euglycemic clamp procedure in conjunction with stable isotopically labeled glucose and palmitate tracer infusions and 18F-fluorodeoxyglucose injection and positron emission tomography to quantify multi-organ insulin action an

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40

Linn, Thomas, Britta Fischer, Nedim Soydan, et al. "Nocturnal Glucose Metabolism after Bedtime Injection of Insulin Glargine or Neutral Protamine Hagedorn Insulin in Patients with Type 2 Diabetes." Journal of Clinical Endocrinology & Metabolism 93, no. 10 (2008): 3839–46. http://dx.doi.org/10.1210/jc.2007-2871.

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Aims/Hypothesis: Insulin glargine is a long-acting human insulin analog often administered at bedtime to patients with type 2 diabetes. It reduces fasting blood glucose levels more efficiently and with less nocturnal hypoglycemic events compared with human neutral protamine Hagedorn (NPH) insulin. Therefore, bedtime injections of insulin glargine and NPH insulin were compared overnight and in the morning. Methods: In 10 type 2 diabetic patients, euglycemic clamps were performed, including [6,6′]2H2 glucose, to study the rate of disappearance (Rd) and endogenous production (EGP) of glucose duri

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41

Szablewski, Leszek. "Changes in Cells Associated with Insulin Resistance." International Journal of Molecular Sciences 25, no. 4 (2024): 2397. http://dx.doi.org/10.3390/ijms25042397.

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Insulin is a polypeptide hormone synthesized and secreted by pancreatic β-cells. It plays an important role as a metabolic hormone. Insulin influences the metabolism of glucose, regulating plasma glucose levels and stimulating glucose storage in organs such as the liver, muscles and adipose tissue. It is involved in fat metabolism, increasing the storage of triglycerides and decreasing lipolysis. Ketone body metabolism also depends on insulin action, as insulin reduces ketone body concentrations and influences protein metabolism. It increases nitrogen retention, facilitates the transport of am

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42

Delgado Mendoza, Roberth Fernando, Dayana Jamileth Aguayo Palma, and Nereida Josefina Valero Cedeño. "CORTISOL Y METABOLISMO GLUCÍDICO EN ADULTOS." Enfermería Investiga 7, no. 4 (2022): 68–73. http://dx.doi.org/10.31243/ei.uta.v7i4.1870.2022.

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El cortisol, es una hormona esteroidea secretada por la corteza suprarrenal, liberada al torrente sanguíneo realiza su función en los tejidos periféricos y regula una amplia gama de procesos corporales, entre ellos la intolerancia de la glucosa y reducción de la sensibilidad a la insulina. La finalidad del presente estudio fue analizar la relación entre los niveles de cortisol y el metabolismo glucídico en adultos. Estudio de diseño documental descriptivo, llevado a cabo mediante una revisión bibliográfica de artículos originales, de revisión, de casos clínicos, entre otros, en revistas indexa

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Salaheldeen, Elsaid, Alexa Jaume, and Sonia Michael Najjar. "Carcinoembryonic Cell Adhesion-Related Molecule 2 Regulates Insulin Secretion and Energy Balance." International Journal of Molecular Sciences 20, no. 13 (2019): 3231. http://dx.doi.org/10.3390/ijms20133231.

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The Carcinoembryonic Antigen-Related Cell Adhesion Molecule (CEACAM) family of proteins plays a significant role in regulating peripheral insulin action by participating in the regulation of insulin metabolism and energy balance. In light of their differential expression, CEACAM1 regulates chiefly insulin extraction, whereas CEACAM2 appears to play a more important role in regulating insulin secretion and overall energy balance, including food intake, energy expenditure and spontaneous physical activity. We will focus this review on the role of CEACAM2 in regulating insulin metabolism and ener

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Darawadi, Bhuvana. "Role of Tumor Suppressor P53 Family in Glucose Metabolism in Association with Diabetes." Advances in Cancer Chemotherapy and Pharmacology 1, no. 1 (2023): 1–7. http://dx.doi.org/10.23880/accp-16000101.

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Subsequent manuscripts have shown that p53, a 391 amino acid protein, was associated with tumour suppression by inducing cell cycle arrest, senescence, or programmed cell death, and mainly focused on oncology. But recent studies are proclaiming that the p53 family of genes is also associated with regulating the balance of the glucose uptake via the many glucose transporters by directly repressing the expression of the GLUT1 & GLUT4, use of glycolysis and oxidative phosphorylation. The p53 regulates phenotypes of diabetes as it is interjecting in many points in regulating the pancreatic fun

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Mikhail, Nasser. "Insulin U-500, the Practical Solution for the treatment of Patients with High Insulin Requirements." Current Diabetes Reviews 17, no. 1 (2020): 26–29. http://dx.doi.org/10.2174/1573399816666200408084614.

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Background: Human regular insulin 500 (U-500) is 5 five times more concentrated than the traditional regular human insulin (U-100). Thus, every 1 ml of U-500 contains 500 units of insulin as opposed to 100 units/ml with most types of insulin. Methods: Review of all the relevant clinical studies related to insulin U-500 until February 12, 2020. Results: Insulin U-500 is indicated in patients with type 2 diabetes who require more than 200 units of insulin per day. Insulin U-500 has both prandial and basal actions, and can be injected as monotherapy in a convenient twice-daily regimen. Available

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Lee, Seung-Hwan, and Kun-Ho Yoon. "A Century of Progress in Diabetes Care with Insulin: A History of Innovations and Foundation for the Future." Diabetes & Metabolism Journal 45, no. 5 (2021): 629–40. http://dx.doi.org/10.4093/dmj.2021.0163.

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The year 2021 marks the 100th anniversary of the discovery of insulin, which has greatly changed the lives of people with diabetes and become a cornerstone of advances in medical science. A rapid bench-to-bedside application of the lifesaving pancreatic extract and its immediate commercialization was the result of a promising idea, positive drive, perseverance, and collaboration of Banting and colleagues. As one of the very few proteins isolated in a pure form at that time, insulin also played a key role in the development of important methodologies and in the beginning of various fields of mo

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Inman, Taylor R., Erika Plyushko, Nicholas P. Austin, and Jeremy L. Johnson. "The role of basal insulin and GLP-1 receptor agonist combination products in the management of type 2 diabetes." Therapeutic Advances in Endocrinology and Metabolism 9, no. 5 (2018): 151–55. http://dx.doi.org/10.1177/2042018818763698.

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The prevalence of type 2 diabetes necessitates the development of new treatment options to individualize therapy. Basal insulin has been a standard treatment option for years, while glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have grown in use over the past decade due to glucose-lowering efficacy and weight loss potential. There are two new combination injectable products that have recently been approved combining basal insulins with GLP-1 RAs in single pen-injector devices. United States guidelines recently emphasize the option to use combination injectable therapy with GLP-1 RAs an

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Newsholme, P., K. Bender, A. Kiely, and L. Brennan. "Amino acid metabolism, insulin secretion and diabetes." Biochemical Society Transactions 35, no. 5 (2007): 1180–86. http://dx.doi.org/10.1042/bst0351180.

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In addition to the primary stimulus of glucose, specific amino acids may acutely and chronically regulate insulin secretion from pancreatic β-cells in vivo and in vitro. Mitochondrial metabolism is crucial for the coupling of glucose, alanine, glutamine and glutamate recognition with exocytosis of insulin granules. This is illustrated by in vitro and in vivo observations discussed in the present review. Mitochondria generate ATP (the main coupling messenger in insulin secretion) and other factors that serve as sensors for the control of the exocytotic process. The main factors that mediate the

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Rebelos, Eleni, Juha O. Rinne, Pirjo Nuutila, and Laura L. Ekblad. "Brain Glucose Metabolism in Health, Obesity, and Cognitive Decline—Does Insulin Have Anything to Do with It? A Narrative Review." Journal of Clinical Medicine 10, no. 7 (2021): 1532. http://dx.doi.org/10.3390/jcm10071532.

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Imaging brain glucose metabolism with fluorine-labelled fluorodeoxyglucose ([18F]-FDG) positron emission tomography (PET) has long been utilized to aid the diagnosis of memory disorders, in particular in differentiating Alzheimer’s disease (AD) from other neurological conditions causing cognitive decline. The interest for studying brain glucose metabolism in the context of metabolic disorders has arisen more recently. Obesity and type 2 diabetes—two diseases characterized by systemic insulin resistance—are associated with an increased risk for AD. Along with the well-defined patterns of fastin

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Danne, Thomas, and Jan Bolinder. "New Insulins and Insulin Therapy." Diabetes Technology & Therapeutics 15, S1 (2013): S—40—S—47. http://dx.doi.org/10.1089/dia.2013.1505.

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