New concepts of glucose-induced insulin secretion in the development of type 2 diabetes: clinical implications
https://doi.org/10.14341/DM2015323-31
Abstract
The prevalence of type 2 diabetes is increasing dramatically, and the pathogenesis of the disease has been studied extensively in recent years. Of particular interest, incretins are reported to cause changes in insulin secretion that affect the natural development of the disease. The emergence of new drugs that act via the incretin axis have led many clinicians to consider their place in clinical practice.
About the Authors
Ivan Ivanovich Dedov
Endocrinology Research Centre, Moscow
Russian Federation
MD, PhD, Professor, Academician of Russian academy of sciences, Director of Endocrinology research centre
Russian Federation
MD, PhD, Professor, Academician of Russian academy of sciences, Director of Endocrinology research centre
Olga Michailovna Smirnova
Endocrinology Research Centre, Moscow; Sechenov First Moscow State Medical University
Russian Federation
Competing Interests: Авторы декларируют отсутствие двойственности (конфликта интересов) при написании данной статьи
Russian Federation
MD, PhD, Professor, General research associate, Department of Program Education and Treatment, Endocrinology Research Centre; Department of Endocrinology and Diabetology, Pediatric Faculty, I.M.Sechenov First Moscow State Medical University
Competing Interests: Авторы декларируют отсутствие двойственности (конфликта интересов) при написании данной статьи
Kononenko Vladimirovna Irina
Endocrinology Research Centre, Moscow, Russian Federation
Russian Federation
Competing Interests: Авторы декларируют отсутствие двойственности (конфликта интересов) при написании данной статьи
Russian Federation
MD, PhD, Leading research associate, Department of Program Education and Treatment, Endocrinology Research Centre; associate professor, Department of Endocrinology and Diabetology, Pediatric Faculty, I.M.Sechenov First Moscow State Medical University
Competing Interests: Авторы декларируют отсутствие двойственности (конфликта интересов) при написании данной статьи
References
1. IDF Diabetes Atlas. 7-th edition, 2014. Available from: http://www.idf.org/diabetesatlas
2. Ткачук В.А., Воротников А.В. Молекулярные механизмы развития резистентности к инсулину. // Сахарный диабет. – 2014. – Т. 17. – №2 – С.29-40. [Tkachuk VA, Vorotnikov AV. Molecular Mechanisms of Insulin Resistance Development. Diabetes mellitus. 2014;17(2):29-40.] doi: 10.14341/DM2014229-40
3. DeFronzo RA, Bonadonna RC, Ferrannini E. Pathogenesis of NIDDM. A balanced overview. Diabetes Care. 1992;15(3):318-368. doi: 10.2337/diacare.15.3.318
4. Weigle DS. Pulsatile secretion of fuel-regulatory hormones. Diabetes. 1987;36(6):764–775. doi: 10.2337/diab.36.6.764
5. Lefèbvre PJ, Paolisso G, Scheen AJ, et al. Pulsatility of insulin and glucagon release: physiological significance and pharmacological implications. Diabetologia. 1987;30(7):443–452. doi: 10.1007/BF00279610
6. Pfeifer MA, Halter JB, Porte D, Jr. Insulin secretion in diabetes mellitus. The American journal of medicine.70(3):579-588. doi: 10.1016/0002-9343(81)90579-9
7. Rorsman P, Renström E. Insulin granule dynamics in pancreatic beta cells. Diabetologia. 2003;46(8):1029–1045. doi: 10.1007/s00125-003-1153-1
8. Axelrod D. Selective imaging of surface fluorescence with very high aperture microscope objectives. J Biomed Opt. 2001;6(1):6–13. doi: 10.1117/1.1335689
9. Tsuboi T, Zhao C, Terakawa S, et al. Simultaneous evanescent wave imaging of insulin vesicle membrane and cargo during a single exocytotic event. Curr Biol. 2000;10(20):1307–1310. doi: 10.1016/S0960-9822(00)00756-9
10. Seino S, Shibasaki T, Minami K. Dinamics of insulin secretin and the clinical implication for obesity and diabetes. J Clin Invest. 2011;121(6):2118-25. doi: 10.1172/JCI45680
11. Wollheim CB, Sharp GW. Regulation of insulin release by calcium. Physiol Rev. 1981;61(4):914–973.
12. Ashcroft FM. ATP-sensitive potassium channelopathies: focus on insulin secretion. J Clin Invest. 2005;115(8):2047–2058. doi: 10.1172/JCI25495
13. Miki T, Nagashima K, Tashiro F, et al. Defective insulin secretion and enhanced insulin action in KATP channel-deficient mice. Proc Natl Acad Sci USA. 1998;95(18):10402-10406. doi: 10.1073/pnas.95.18.10402
14. Seghers V, Nakazaki M, DeMayo F,et al. Sur1 knockout mice. A model for K(ATP) channel-independent regulation of insulin secretion. J Biol Chem. 2000;275(13):9270-9277. doi: 10.1074/jbc.275.13.9270
15. Nauck MA. Unraveling the science of incretin biology. Am J Med. 2009;122(6 Suppl):S3-S10. doi: 10.1016/j.amjmed.2009.03.012
16. Yasuda K, Inagaki N, Yamada Y, et al. Hamster gastric inhibitory polypeptide receptor expressed in pancreatic islets and clonal insulin-secreting cells: its structure and functional properties. Biochem Biophys Res Commun. 1994;205(3):1556-1562. doi: 10.1006/bbrc.1994.2844
17. Fujimoto W, Miki T, Ogura T, et al. Niflumic acid-sensitive ion channels play an important role in the induction of glucose-stimulated insulin secretion by cyclic AMP in mice. Diabetologia. 2009;52(5):863-872. doi: 10.1007/s00125-009-1306-y
18. Takahashi T, Shibasaki T, Takahashi H, et al. Antidiabetic Sulfonylureas and cAMP Cooperatively Activate Epac2A. Sci Signal. 2013;6(298):ra94. doi: 10.1126/scisignal.2004581
19. Marre M, Shaw J, Brändle M, et al. Liraglutide, a once-daily human GLP-1 analogue, added to a sulphonylurea over 26 weeks produces greater improvements in glycaemic and weight control compared with adding rosiglitazone or placebo in subjects with Type 2 diabetes (LEAD-1 SU). Diabet Med. 2009;26(3):268-278. doi: 10.1111/j.1464-5491.2009.02666.x
20. Kubota A, Maeda H1, Kanamori A, et al. Efficacy and safety of sitagliptin monotherapy and combination therapy in Japanese type 2 diabetes patients. J Diabetes Investig. 2012 20;3(6):503-509. doi: 10.1111/j.2040-1124.2012.00221.x
21. Yabe D, Seino Y. Dipeptidyl peptidase-4 inhibitors and sulfonylureas for type 2 diabetes: Friend or foe? J Diabetes Investig. 2014;5(5):475-7. doi: 10.1111/jdi.12229
22. Takahashi H, Shibasaki T, Park JH, et al. Role of Epac2A/Rap1 signaling in interplay between incretin and sulfonylurea in insulin secretion. Diabetes. 2015;64(4):1262-1272. doi: 10.2337/db14-0576
23. Zhang CL, Katoh M, Shibasaki T, et al. The cAMP sensor Epac2 is a direct target of antidiabetic sulfonylurea drugs. Science. 2009;325(5940):607-10. doi: 10.1126/science.1172256
24. Seino Y, Yabe D. GIP and GLP-1: incretin actions beyond pancreas. J Diabetes Investig. 2013;4(2):108-130. doi: 10.1111/jdi.12065
25. Mukai E, Ishida H, Kato S, et al. Metabolic inhibition impairs ATP-sensitive K+ channel block by sulfonylurea in pancreatic beta-cells. Am J Physiol. 1998;274(1 Pt 1):E38-44.
Supplementary files
Review
For citations:
Dedov I.I., Smirnova O.M., Irina K.V. New concepts of glucose-induced insulin secretion in the development of type 2 diabetes: clinical implications. Diabetes mellitus. 2015;18(3):23-31. (In Russ.) https://doi.org/10.14341/DM2015323-31
Views:
4235
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND 4.0).
Email this article 
