Diyabette Leptin Hormonun Olası Etkileri

Yıl 2019, Cilt: 7 Sayı: 3, 1969 - 1975, 31.07.2019

Eylem Taşkın Güven , Celal Güven , Salih Tunç Kaya , Yusuf Sevgiler

https://doi.org/10.29130/dubited.578925

Öz

Şeker
hastalığı olarak bilinen diyabet, çeşitli komplikasyonları (kalp ve dolaşım
hastalıkları, kanser ve buna benzer hastalıklar) beraberinde getiren, insan
hayatını olumsuz yönde etkileyen metabolik bir hastalıktır. Genel olarak diyabet
tip I ve tip II olmak üzere iki büyük alt grupta toplanan bir hastalıktır. Tip I
diyabette beta (β) hücrelerinin apoptoz ile kaybı insülin salgısının
azalmasında önemli bir mekanizmadır. Leptin de insülin gibi antiapoptotik ve
proliferatif hormonlardan biridir. Dahası düşük leptin ve insülin tedavisinin
sadece yüksek doz insülin kullanımına oranla kan şekerinin tamponlanmasında
daha etkili olduğu bildirilmektedir. Fakat leptinin tip I diyabetteki bu
etkisi/etkileri hala gizemini korumaktadır. Leptinin tip I diyabetteki önemli
etkisinden biri de yağların β oksidasyonunun artmasına neden olarak, kan
şekerinin tamponlanmasını da sağları. Bu da insülin direncinin oluşmasının
azalmasına neden olmaktadır. Ayrıca leptinin insülinin anabolik etkilerini
taklit ettiği gibi diyabette meydana gelen ketoasidozu önlediği de
vurgulanmaktadır. Dolayısıyla leptin tedavisi, zorunlu yüksek doz insülin
kullanımı azaltılmasına olanak tanıyabilmektedir. Bu derleme, literatürdeki
leptin ve diyabet arasındaki

Anahtar Kelimeler

Leptin, Diyabet, Oksidatif stres, İnsülin, Apoptozis, Aktin filamentleri, ATP'ye duyarlı potasyum kanalları

The Possible Effects of Leptin Hormone in Diabetes

Öz

Diabetes, known as a disorder of glucose, is a
metabolic disease that brings about various complications (cardiovascular and
circulatory disorder, cancer, and similar diseases) and affects human life
negatively. Diabetes is a disease that has two big sub-categories as type I and
type II. Beta (β) cell loss by apoptosis in type I diabetics is an important
mechanism in the decrease of insulin secretion. Like insulin, leptin is also
one of the anti-apoptotic and proliferative hormones. Moreover, it is known
that low leptin and insulin treatment are more effective in tamponing blood
glucose than only high dose of insulin use. However, this effect/these effects
of type I diabetics still keeps its mystery. Another significant effect of
leptin in type I diabetes is to tampon blood glucose by increasing in fat oxidation.
Moreover, this causes a decrease in insulin resistance. In addition, it is
emphasized that leptin not only imitates anabolic effects of insulin but also avoids
ketoacidosis that occurs in diabetes. Consequently, leptin treatment enables a
decrease in high dose of insulin use. The evidence to be obtained has a potential to help enlighten this
complicated relationship between leptin and diabetes in literature by the
review.

Anahtar Kelimeler

Leptin, Diabetes, Oxidative stress, Insulin, Apoptosis, Actin filaments, ATP sensitive potassium channels

Kaynakça

• [1] S. Wild, G. Roglic, A. Green, R. Sicree and H. King, “Global prevalence of diabetes: estimates for the year 2000 and projections for 2030,” Diabetes Care, vol. 27, no. 5, pp. 1047-1053, 2004.
• [2] J. M. Forbes and M. E. Cooper, “Mechanisms of diabetic complications,” Physiol Rev, vol. 93, no. 1, pp. 137-188, 2013.
• [3] J. B. Buse, S. Caprio, W. T. Cefalu, A. Ceriello, S. Del Prato, S. E. Inzucchi, S. McLaughlin, G. L. Phillips, 2nd, R. P. Robertson, F. Rubino, R. Kahn and M. S. Kirkman, “How do we define cure of diabetes?,” Diabetes Care, vol. 32, no. 11, pp. 2133-2135, 2009.
• [4] R. F. de Wilde, B. H. Edil, R. H. Hruban and A. Maitra, “Well-differentiated pancreatic neuroendocrine tumors: from genetics to therapy,” Nat Rev Gastroenterol Hepatol, vol. 9, no. 4, pp. 199-208, 2012.
• [5] S. Kawamoto, P. T. Johnson, C. Shi, A. D. Singhi, R. H. Hruban, C. L. Wolfgang, B. H. Edil and E. K. Fishman, “Pancreatic neuroendocrine tumor with cystlike changes: evaluation with MDCT,” AJR Am J Roentgenol, vol. 200, no. 3, pp. W283-290, 2013.
• [6] L. M. Dickson and C. J. Rhodes, “Pancreatic beta-cell growth and survival in the onset of type 2 diabetes: a role for protein kinase B in the Akt?,” Am J Physiol Endocrinol Metab, vol. 287, no. 2, pp. E192-198, 2004.
• [7] F. Zhang, Y. Chen, M. Heiman and R. Dimarchi, “Leptin: structure, function and biology,” Vitam Horm, vol. 71, no. pp. 345-372, 2005.
• [8] O. Moran and M. Phillip, “Leptin: obesity, diabetes and other peripheral effects--a review,” Pediatr Diabetes, vol. 4, no. 2, pp. 101-109, 2003.
• [9] R. S. Ahima and S. Y. Osei, “Leptin signaling,” Physiol Behav, vol. 81, no. 2, pp. 223-241, 2004.
• [10] L. Huang and C. Li, “Leptin: a multifunctional hormone,” Cell Res, vol. 10, no. 2, pp. 81-92, 2000.
• [11] I. C. McMillen and J. S. Robinson, “Developmental origins of the metabolic syndrome: prediction, plasticity, and programming,” Physiol Rev, vol. 85, no. 2, pp. 571-633, 2005.
• [12] L. L. Bellinger and L. L. Bernardis, “The dorsomedial hypothalamic nucleus and its role in ingestive behavior and body weight regulation: lessons learned from lesioning studies,” Physiol Behav, vol. 76, no. 3, pp. 431-442, 2002.
• [13] I. Kelesidis and C. S. Mantzoros, “Leptin and its emerging role in children and adolescents,” Clin Pediatr Endocrinol, vol. 15, no. 1, pp. 1-14, 2006.
• [14] T. Kelesidis and C. S. Mantzoros, “The emerging role of leptin in humans,” Pediatr Endocrinol Rev, vol. 3, no. 3, pp. 239-248, 2006.
• [15] F. Malli, A. I. Papaioannou, K. I. Gourgoulianis and Z. Daniil, “The role of leptin in the respiratory system: an overview,” Respir Res, vol. 11, no. pp. 152, 2010.
• [16] P. Schling and G. Loffler, “Cross talk between adipose tissue cells: impact on pathophysiology,” News Physiol Sci, vol. 17, no. pp. 99-104, 2002.
• [17] X. D. Chen, T. Lei, T. Xia, L. Gan and Z. Q. Yang, “Increased expression of resistin and tumour necrosis factor-alpha in pig adipose tissue as well as effect of feeding treatment on resistin and cAMP pathway,” Diabetes Obes Metab, vol. 6, no. 4, pp. 271-279, 2004.
• [18] B. E. Wisse, K. Ogimoto, G. J. Morton, C. W. Wilkinson, R. S. Frayo, D. E. Cummings and M. W. Schwartz, “Physiological regulation of hypothalamic IL-1beta gene expression by leptin and glucocorticoids: implications for energy homeostasis,” Am J Physiol Endocrinol Metab, vol. 287, no. 6, pp. E1107-1113, 2004.
• [19] S. Fernandez-Veledo, I. Nieto-Vazquez, J. de Castro, M. P. Ramos, S. Bruderlein, P. Moller and M. Lorenzo, “Hyperinsulinemia induces insulin resistance on glucose and lipid metabolism in a human adipocytic cell line: paracrine interaction with myocytes,” J Clin Endocrinol Metab, vol. 93, no. 7, pp. 2866-2876, 2008.
• [20] P. Cettour-Rose, C. Theander-Carrillo, C. Asensio, M. Klein, T. J. Visser, A. G. Burger, C. A. Meier and F. Rohner-Jeanrenaud, “Hypothyroidism in rats decreases peripheral glucose utilisation, a defect partially corrected by central leptin infusion,” Diabetologia, vol. 48, no. 4, pp. 624-633, 2005.
• [21] L. Marroqui, A. Gonzalez, P. Neco, E. Caballero-Garrido, E. Vieira, C. Ripoll, A. Nadal and I. Quesada, “Role of leptin in the pancreatic beta-cell: effects and signaling pathways,” J Mol Endocrinol, vol. 49, no. 1, pp. R9-17, 2012.
• [22] J. S. McTaggart, R. H. Clark and F. M. Ashcroft, “The role of the KATP channel in glucose homeostasis in health and disease: more than meets the islet,” J Physiol, vol. 588, no. Pt 17, pp. 3201-3209, 2010.
• [23] A. Nakbi, N. Koubaa, K. Ben Hamda, S. Hammami, N. Attia, R. Boumiza, A. Miled, M. Ben Farhat and M. Hammami, “[Association between oxidative stress parameters and inflammation markers according to the gravity of the acute coronary syndrome],” Tunis Med, vol. 89, no. 7, pp. 621-626, 2011.
• [24] L. Wang, S. Gao, W. Jiang, C. Luo, M. Xu, L. Bohlin, M. Rosendahl and W. Huang, “Antioxidative dietary compounds modulate gene expression associated with apoptosis, DNA repair, inhibition of cell proliferation and migration,” Int J Mol Sci, vol. 15, no. 9, pp. 16226-16245, 2014.
• [25] J. H. Rubenstein, H. Morgenstern, D. McConell, J. M. Scheiman, P. Schoenfeld, H. Appelman, L. F. McMahon, Jr., J. Y. Kao, V. Metko, M. Zhang and J. M. Inadomi, “Associations of diabetes mellitus, insulin, leptin, and ghrelin with gastroesophageal reflux and Barrett's esophagus,” Gastroenterology, vol. 145, no. 6, pp. 1237-1244 e1231-1235, 2013.
• [26] K. Tucholski and E. Otto-Buczkowska, “The role of leptin in the regulation of carbohydrate metabolism,” Endokrynol Pol, vol. 62, no. 3, pp. 258-262, 2011.
• [27] T. Fujikawa, J. C. Chuang, I. Sakata, G. Ramadori and R. Coppari, “Leptin therapy improves insulin-deficient type 1 diabetes by CNS-dependent mechanisms in mice,” Proc Natl Acad Sci U S A, vol. 107, no. 40, pp. 17391-17396, 2010.
• [28] M. Y. Wang, L. Chen, G. O. Clark, Y. Lee, R. D. Stevens, O. R. Ilkayeva, B. R. Wenner, J. R. Bain, M. J. Charron, C. B. Newgard and R. H. Unger, “Leptin therapy in insulin-deficient type I diabetes,” Proc Natl Acad Sci U S A, vol. 107, no. 11, pp. 4813-4819, 2010.
• [29] H. C. Denroche, W. L. Quong, J. E. Bruin, E. Tuduri, A. Asadi, M. M. Glavas, J. K. Fox and T. J. Kieffer, “Leptin administration enhances islet transplant performance in diabetic mice,” Diabetes, vol. 62, no. 8, pp. 2738-2746, 2013.
• [30] T. Sakai, T. Kusakabe, K. Ebihara, D. Aotani, S. Yamamoto-Kataoka, M. Zhao, V. M. Gumbilai, C. Ebihara, M. Aizawa-Abe, Y. Yamamoto, M. Noguchi, J. Fujikura, K. Hosoda, N. Inagaki and K. Nakao, “Leptin restores the insulinotropic effect of exenatide in a mouse model of type 2 diabetes with increased adiposity induced by streptozotocin and high-fat diet,” Am J Physiol Endocrinol Metab, vol. 307, no. 8, pp. E712-719, 2014.
• [31] H. S. Moon, M. Dalamaga, S. Y. Kim, S. A. Polyzos, O. P. Hamnvik, F. Magkos, J. Paruthi and C. S. Mantzoros, “Leptin's role in lipodystrophic and nonlipodystrophic insulin-resistant and diabetic individuals,” Endocr Rev, vol. 34, no. 3, pp. 377-412, 2013.