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Journal articles on the topic 'Insulin action'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 July 2025

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1

Meyts, Pierre De, Claus T. Christoffersen, Hans Tornqvist, and Klaus Seedorf. "Insulin receptors and insulin action." Current Opinion in Endocrinology and Diabetes 3, no. 5 (1996): 1. http://dx.doi.org/10.1097/00060793-199610000-00003.

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2

Kucera, Michelle L., and John P. Graham. "Insulin Lispro, a New Insulin Analog." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 18, no. 3 (1998): 526–38. http://dx.doi.org/10.1002/j.1875-9114.1998.tb03116.x.

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Insulin lispro is a rapid‐acting insulin analog to regular insulin. Inversion of the proline‐lysine amino acid sequence at positions 28 and 29 on the B chain is responsible for its more rapid absorption, faster onset, and shorter duration of action compared with regular insulin. The fast onset of action allows for greater flexibility in dosing and mealtime scheduling. Insulin lispro provides equivalent or slightly improved glycemic control in patients with types I and II diabetes mellitus compared with regular insulin, without subsequent increases in hypoglycemic episodes. It also results in g

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3

Bailey, CJ. "Improved Insulin Action." Emerging Therapeutic Targets 1, no. 1 (1997): 229–33. http://dx.doi.org/10.1517/14728222.1.1.229.

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4

Taylor, Roy. "Insulin action 1991." Clinical Endocrinology 34, no. 2 (1991): 159–71. http://dx.doi.org/10.1111/j.1365-2265.1991.tb00287.x.

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5

Hausmann, Simone, and Siegfried Ussar. "Insulin receptor trafficking steers insulin action." Molecular Metabolism 5, no. 4 (2016): 253–54. http://dx.doi.org/10.1016/j.molmet.2016.02.004.

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6

Dedov, I. I., and M. V. Shestakova. "On the centenary of the insulin discovery." Diabetes mellitus 24, no. 1 (2021): 11–16. http://dx.doi.org/10.14341/dm12733.

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The discovery of insulin and the beginning of its use in 1921–1922 made a revolution in endocrinology and in medicine in general. This significant event gave millions of patients with diabetes not only the opportunity to live, but also the hope that their life with this disease would be full.The article examines the history of insulin discovery, as well as the evolution of several generations of insulin preparations and the advantages of each of the generations that have radically changed not only life expectancy, but also its quality.The first generation — insulins of animal origin and the so

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7

Liu, Jia, and Zhenqi Liu. "Muscle Insulin Resistance and the Inflamed Microvasculature: Fire from Within." International Journal of Molecular Sciences 20, no. 3 (2019): 562. http://dx.doi.org/10.3390/ijms20030562.

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Insulin is a vascular hormone and regulates vascular tone and reactivity. Muscle is a major insulin target that is responsible for the majority of insulin-stimulated glucose use. Evidence confirms that muscle microvasculature is an important insulin action site and critically regulates insulin delivery to muscle and action on myocytes, thereby affecting insulin-mediated glucose disposal. Insulin via activation of its signaling cascade in the endothelial cells increases muscle microvascular perfusion, which leads to an expansion of the endothelial exchange surface area. Insulin’s microvascular

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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

Ming, Zhi, and W. Wayne Lautt. "HISS, not insulin, causes vasodilation in response to administered insulin." Journal of Applied Physiology 110, no. 1 (2011): 60–68. http://dx.doi.org/10.1152/japplphysiol.00714.2010.

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Meal-induced sensitization to the dynamic actions of insulin results from the peripheral actions of a hormone released by the liver (hepatic insulin sensitizing substance or HISS). Absence of meal-induced insulin sensitization results in the pathologies associated with cardiometabolic risk. Using three protocols that have previously demonstrated HISS metabolic action, we tested the hypothesis that HISS accounts for the vasodilation that has been associated with insulin. The dynamic metabolic actions of insulin and HISS were determined using a euglycemic clamp in response to a bolus of 100 mU/k

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10

Cheatham, B. "Insulin action and the insulin signaling network." Endocrine Reviews 16, no. 2 (1995): 117–42. http://dx.doi.org/10.1210/er.16.2.117.

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11

CHEATHAM, BENTLEY, and C. RONALD KAHN. "Insulin Action and the Insulin Signaling Network*." Endocrine Reviews 16, no. 2 (1995): 117–42. http://dx.doi.org/10.1210/edrv-16-2-117.

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12

Timothy Garvey, W., and Morris J. Birnbaum. "1 Cellular insulin action and insulin resistance." Baillière's Clinical Endocrinology and Metabolism 7, no. 4 (1993): 785–873. http://dx.doi.org/10.1016/s0950-351x(05)80237-x.

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13

Heinemann, Lutz, and James H. Anderson. "Measurement of Insulin Absorption and Insulin Action." Diabetes Technology & Therapeutics 6, no. 5 (2004): 698–718. http://dx.doi.org/10.1089/dia.2004.6.698.

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14

Heinemann, Lutz. "Variability of Insulin Absorption and Insulin Action." Diabetes Technology & Therapeutics 4, no. 5 (2002): 673–82. http://dx.doi.org/10.1089/152091502320798312.

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15

Petersen, Max C., and Gerald I. Shulman. "Mechanisms of Insulin Action and Insulin Resistance." Physiological Reviews 98, no. 4 (2018): 2133–223. http://dx.doi.org/10.1152/physrev.00063.2017.

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The 1921 discovery of insulin was a Big Bang from which a vast and expanding universe of research into insulin action and resistance has issued. In the intervening century, some discoveries have matured, coalescing into solid and fertile ground for clinical application; others remain incompletely investigated and scientifically controversial. Here, we attempt to synthesize this work to guide further mechanistic investigation and to inform the development of novel therapies for type 2 diabetes (T2D). The rational development of such therapies necessitates detailed knowledge of one of the key pa

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16

McKane, W. R., A. B. Stevens, T. M. Ferguson, et al. "Insulin Secretion and Insulin Action in Hypertriglyceridaemia." Clinical Science 74, s18 (1988): 10P. http://dx.doi.org/10.1042/cs074010pb.

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17

Tsakiridis, Theodoros, Peter Tong, Benjamin Matthews, et al. "Role of the actin cytoskeleton in insulin action." Microscopy Research and Technique 47, no. 2 (1999): 79–92. http://dx.doi.org/10.1002/(sici)1097-0029(19991015)47:2<79::aid-jemt1>3.0.co;2-s.

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18

Levinson, Randy. "Diabetes: Sensitizing insulin action." Nature Medicine 20, no. 8 (2014): 813. http://dx.doi.org/10.1038/nm.3660.

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19

Mahler, Robert, W. C. Shoemaker, and James Ashmore. "HEPATIC ACTION OF INSULIN." Annals of the New York Academy of Sciences 82, no. 2 (2006): 452–59. http://dx.doi.org/10.1111/j.1749-6632.1959.tb44925.x.

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20

KASUGA, Masato. "Mechanism of Insulin Action." Folia Endocrinologica Japonica 69, no. 10 (1993): 1029–34. http://dx.doi.org/10.1507/endocrine1927.69.10_1029.

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21

Elmendorf, Jeffrey S. "Fluidity of Insulin Action." Molecular Biotechnology 27, no. 2 (2004): 127–38. http://dx.doi.org/10.1385/mb:27:2:127.

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22

Espinal, Joe. "Mechanism of insulin action." Nature 328, no. 6131 (1987): 574–75. http://dx.doi.org/10.1038/328574a0.

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23

Tavaré, J. M., L. M. Fletcher, P. B. Oatey, L. Tyas, J. G. Wakefield, and G. I. Welsh. "Lighting up insulin action." Diabetic Medicine 18, no. 4 (2001): 253–60. http://dx.doi.org/10.1046/j.1464-5491.2001.00540.x.

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24

Fantini, J., and G. Marchis-Mouren. "Mechanisms of insulin action." Biochimie 69, no. 11-12 (1987): 1262. http://dx.doi.org/10.1016/0300-9084(87)90158-1.

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25

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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26

Stöckli, Jacqueline, and David E. James. "Insulin Action under Arrestin." Cell Metabolism 9, no. 3 (2009): 213–14. http://dx.doi.org/10.1016/j.cmet.2009.02.005.

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27

Knights, Alexander J., Alister PW Funnell, Richard CM Pearson, Merlin Crossley, and Kim S. Bell-Anderson. "Adipokines and insulin action." Adipocyte 3, no. 2 (2014): 88–96. http://dx.doi.org/10.4161/adip.27552.

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28

Bleich, David. "Breaking Down Insulin Action." Journal of Clinical Endocrinology & Metabolism 105, no. 6 (2020): e2287-e2288. http://dx.doi.org/10.1210/clinem/dgaa136.

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29

Takeuchi, Setsuya. "Action mode of insulin." Journal of Nippon Medical School 56, no. 4 (1989): 319–28. http://dx.doi.org/10.1272/jnms1923.56.319.

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30

Taylor, R., R. J. Heine, J. Collins, O. F. W. James, and K. G. M. M. Alberti. "Insulin action in cirrhosis." Hepatology 5, no. 1 (1985): 64–71. http://dx.doi.org/10.1002/hep.1840050115.

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31

Pirola, L., A. M. Johnston, and E. Van Obberghen. "Modulation of insulin action." Diabetologia 47, no. 2 (2004): 170–84. http://dx.doi.org/10.1007/s00125-003-1313-3.

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32

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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33

Heinemann, Lutz, Robert Baughman, Anders Boss, and Marcus Hompesch. "Pharmacokinetic and Pharmacodynamic Properties of a Novel Inhaled Insulin." Journal of Diabetes Science and Technology 11, no. 1 (2016): 148–56. http://dx.doi.org/10.1177/1932296816658055.

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Advances in insulin treatment options over recent decades have markedly improved the management of diabetes. Despite this, glycemic control remains suboptimal in many people with diabetes. Although postprandial glucose control has been improved with the development of subcutaneously injected rapid-acting insulin analogs, currently available insulins are not able to fully mimic the physiological time–action profile of endogenously secreted insulin after a meal. The delayed onset of metabolic action and prolonged period of effect induce the risk of postprandial hyperglycemia and late postprandia

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34

Reid, Maria A. G., and W. Wayne Lautt. "Pattern of insulin delivery affects hepatic insulin sensitizing substance (HISS) action and insulin resistance." Canadian Journal of Physiology and Pharmacology 82, no. 12 (2004): 1068–74. http://dx.doi.org/10.1139/y04-111.

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Hepatic insulin sensitizing substance (HISS) action accounts for 55% of the glucose disposal effect of a bolus of insulin in the fed state. To determine the effect of continuous versus pulsatile insulin delivery on HISS action in male Sprague–Dawley rats, insulin sensitivity was assessed using the rapid insulin sensitivity test (RIST) before and after a continuous, pulsatile, or bolus insulin (60 mU/kg i.v.) delivery. There was a significant difference in the RIST index after a continuous insulin infusion (247.9 mg/kg before, 73.2 mg/kg after) but not after 3 pulses where insulin action return

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35

Muniyappa, Ranganath, and Michael J. Quon. "Insulin action and insulin resistance in vascular endothelium." Current Opinion in Clinical Nutrition and Metabolic Care 10, no. 4 (2007): 523–30. http://dx.doi.org/10.1097/mco.0b013e32819f8ecd.

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36

Flatt, Peter R., and Clifford J. Bailey. "Molecular mechanisms of insulin secretion and insulin action." Journal of Biological Education 25, no. 1 (1991): 9–14. http://dx.doi.org/10.1080/00219266.1991.9655167.

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37

Ballotti, R., Y. Le Marchand-Brustel, S. Gammeltoft, and E. Van Obberghen. "Insulin receptor : tyrosine kinase activity and insulin action." Reproduction Nutrition Développement 29, no. 6 (1989): 653–61. http://dx.doi.org/10.1051/rnd:19890603.

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38

James, David E. "Molecular mapping of insulin action and insulin resistance." Diabetes Research and Clinical Practice 120 (October 2016): S23—S24. http://dx.doi.org/10.1016/s0168-8227(16)30947-0.

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39

Saudek, F., T. Pelikánová, V. Bartoš, et al. "Insulin action and insulin binding following pancreas transplantation." Diabetologia 34, S1 (1991): S71—S75. http://dx.doi.org/10.1007/bf00587624.

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40

KOBAYASHI, M., Y. TAKATA, O. ISHIBASHI, et al. "Insulin action in primary defects of insulin receptors." Diabetes Research and Clinical Practice 3 (1987): S11. http://dx.doi.org/10.1016/0168-8227(87)90018-0.

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41

Wang, Nasui, Weidong Chai, Lina Zhao, Lijian Tao, Wenhong Cao, and Zhenqi Liu. "Losartan increases muscle insulin delivery and rescues insulin's metabolic action during lipid infusion via microvascular recruitment." American Journal of Physiology-Endocrinology and Metabolism 304, no. 5 (2013): E538—E545. http://dx.doi.org/10.1152/ajpendo.00537.2012.

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Insulin delivery and transendothelial insulin transport are two discrete steps that limit muscle insulin action. Angiotensin II type 1 receptor (AT1R) blockade recruits microvasculature and increases glucose use in muscle. Increased muscle microvascular perfusion is associated with increased muscle delivery and action of insulin. To examine the effect of acute AT1R blockade on muscle insulin uptake and action, rats were studied after an overnight fast to examine the effects of losartan on muscle insulin uptake ( protocol 1), microvascular perfusion ( protocol 2), and insulin's microvascular an

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42

Sasaki, S. "Insulin Resistance in Ovine Skeletal Muscle; Insulin Binding and Insulin Action." Asian-Australasian Journal of Animal Sciences 2, no. 3 (1989): 218–19. http://dx.doi.org/10.5713/ajas.1989.218.

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43

Schmitz, Ole. "Insulin action and insulin therapy in uremic insulin-dependent diabetic patients." Journal of Diabetic Complications 3, no. 1 (1989): 49–55. http://dx.doi.org/10.1016/0891-6632(89)90011-1.

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44

Froment, Pascal, and Philippe Touraine. "Thiazolidinediones and Fertility in Polycystic Ovary Syndrome (PCOS)." PPAR Research 2006 (2006): 1–8. http://dx.doi.org/10.1155/ppar/2006/73986.

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Polycystic ovary syndrome (PCOS) is the most frequent cause of female infertility. The treatment of PCOS patients with insulin sensitizers, such as metformin or thiazolidinediones, increases the ovulation rate and the number of successful pregnancies. The positive action of the insulin-sensitizing treatments could be explained by a decrease in the peripheral insulin resistance but also by a direct action at the ovarian level. We report in this review different hypotheses of thiazolidinediones actions to improve PCOS (steroid secretion by ovarian cells ; insulin sensitivity in muscle and adipoc

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45

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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46

Thomaseth, K., A. Pavan, G. Pacini, and B. Ahrén. "Glucagon-like peptide-1 accelerates the onset of insulin action on glucose disappearance in mice." American Journal of Physiology-Endocrinology and Metabolism 292, no. 6 (2007): E1808—E1814. http://dx.doi.org/10.1152/ajpendo.00303.2006.

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Glucagon-like peptide-1 (GLP-1) plays a significant role in glucose homeostasis through its incretin effect on insulin secretion. However, GLP-1 also exhibits extrapancreatic actions, and in particular its possible influences on insulin sensitivity are controversial. To study the dynamic action of GLP-1 on insulin sensitivity, we applied advanced statistical modeling methods to study glucose disappearance in mice that underwent intravenous glucose tolerance test with administration of GLP-1 at various dose levels. In particular, the minimal model of glucose disappearance was exploited within a

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47

Heinemann, Lutz, and Christopher G. Parkin. "Rethinking the Viability and Utility of Inhaled Insulin in Clinical Practice." Journal of Diabetes Research 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/4568903.

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Despite considerable advances in pharmacotherapy and self-monitoring technologies in the last decades, a large percentage of adults with diabetes remain unsuccessful in achieving optimal glucose due to suboptimal medication adherence. Contributors to suboptimal adherence to insulin treatment include pain, inconvenience, and regimen complexity; however, a key driver is hypoglycemia. Improvements in the PK/PD characteristics of today’s SC insulins provide more physiologic coverage of basal and prandial insulin requirements than regular human insulin; however, they do not achieve the rapid on/rap

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48

Kahn, S. E., R. N. Bergman, M. W. Schwartz, G. J. Taborsky, and D. Porte. "Short-term hyperglycemia and hyperinsulinemia improve insulin action but do not alter glucose action in normal humans." American Journal of Physiology-Endocrinology and Metabolism 262, no. 4 (1992): E518—E523. http://dx.doi.org/10.1152/ajpendo.1992.262.4.e518.

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Tissue glucose uptake occurs by insulin-dependent and insulin-independent mechanisms. To evaluate the effect of mild hyperglycemia and hyperinsulinemia on the parameters responsible for glucose disposal, glucose (1.17 mmol/min) or saline was infused into six healthy male subjects (age 25-38 yr, body mass index 22.1-26.3 kg/m2) for 24 h. Thereafter, while the infusion continued, indexes of insulin sensitivity (SI), glucose effectiveness at basal insulin (SG), basal insulin effect (BIE = SI x basal insulin), and glucose effectiveness at zero insulin (GEZI = SG - BIE) were measured using Bergman'

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49

Sánchez-Margalet, Víctor, and Carmen González-Yanes. "Pancreastatin inhibits insulin action in rat adipocytes." American Journal of Physiology-Endocrinology and Metabolism 275, no. 6 (1998): E1055—E1060. http://dx.doi.org/10.1152/ajpendo.1998.275.6.e1055.

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Pancreastatin (PST), a regulatory peptide with a general inhibitory effect on secretion, is derived from chromogranin A, a glycoprotein present throughout the neuroendocrine system. We have previously demonstrated the counterregulatory role of PST on insulin action in rat hepatocytes. Here, we are reporting the PST effects on rat adipocytes. PST dose dependently inhibits basal and insulin-stimulated glucose transport, lactate production, and lipogenesis, impairing the main metabolic actions of insulin in adipocytes. These effects were observed in a wide range of insulin concentrations, leading

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50

Dela, Flemming, Mads Holten, and Christina Merete Rørvig Jensen. "Insulin Action, Training, and Aging." International Journal of Sport Nutrition and Exercise Metabolism 11, s1 (2001): S78—S85. http://dx.doi.org/10.1123/ijsnem.11.s1.s78.

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