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International Journal of Latest Research in Science and Technology

DOI:10.29111/ijlrst   ISRA Impact Factor:3.35,  Peer-reviewed, Open-access Journal

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INSULIN GENE EXPRESSION AND ITS DETECTION IN THE KIDNEYS OF RATS WITH IMPAIRED GLUCOSE TOLERANCE

Research Paper Open Access

International Journal of Latest Research in Science and Technology Vol.4 Issue 2, pp 171-179,Year 2015

INSULIN GENE EXPRESSION AND ITS DETECTION IN THE KIDNEYS OF RATS WITH IMPAIRED GLUCOSE TOLERANCE

Claudia Soto,JesúsJuárez, Imelda González, Esther Uría,Luis Raya, Mónica Ruiz, Natalia García

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Received : 18 April 2015; Accepted : 25 April 2015 ; Published : 30 April 2015

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Article No. 10515
Abstract

In impairedglucosetolerance (IGT) –a major risk factor for the development of type 2 diabetes mellitus (DM)–reportedcomplicationsincluderetinopathy, renal disease, polyneuropathy and dyslipidemia. Additionally, impaired β cell function has been demonstrated. Renal diseasemay be related to local insulinaction, as itstimulatessodiumreabsorption and nitric oxide production. Recently, we found that rat kidneys are able to produce insulin as well as the Pdx-1 and Nkx6.1 transcription factors, which play a key role in differentiation of β-cells and insulin expression, under standard physiological conditions. In this work, we investigated the expression of insulin and its related transcription factors in the kidneys of rats which were administered a 30% sucrose solution for six months, to induce an IGT model. Theseanimalsshowed a significantdecrease in the renal genicexpression of insulin and itsrelatedtranscriptionfactors and consequently, a decline in itstissuedetectionthroughimmunohistochemistry. Also, IGT animals showed renal tissue damage at the cortex and medulla. In addition to IGT, sucrosetreatedratspresentedhyperinsulinemia, increasedtryglicerides and a decrement in HDL blood levels. We suggest that as in the pancreas, IGT leads to a decline in local insulinproduction in thekidney and thereforeanimpairment in sodiumreabsorption and nitric oxide production. This may contribute to kidney tissue damage.

Key Words   
kidney, insulin, pancreatic transcription factors, Pdx-1, Nkx6.1, impaired glucose toleranc

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References
  1. Tabák AG, Herder C,Rathmann W, Brunner EJ,Kivimäki M.Prediabetes: a high-risk state for diabetes development. Lancet, 2012; 379: 2279–90.
  2. Singleton JR, Smith AG, Russell JW, Feldman EL.Microvascular Complications of Impaired Glucose Tolerance. Diabetes, 2012; 52: 2867-73
  3. Harris MI, Klein R, Welborn TA, Knuiman MW. Onset of NIDDM occurs at least 4–7 years before clinical diagnosis. Diabetes Care, 1992;15: 815–19.
  4. Mykkanen L, Haffner SM, Kuusisto J, Pyorala K, Laakso M. Microalbuminuria precedes the development of NIDDM. Diabetes, 1994;43:552–7.
  5. Faerch K, Vaag A., Holst JJ, Hansen T, Jørgensen T, Borch-Johnsen K. Natural history of insulin sensitivity and insulin secretion in the progression from normal glucose tolerance to impaired fasting glycemia and impaired glucose tolerance: the inter99 study.Diabetes Care, 2009; 32:439-44.
  6. Pratley RE, Weyer C. The role of impaired early insulin secretion in the pathogenesis of type II diabetes mellitus. Diabetologia, 2001;44: 929–45.
  7. Ferrannini E, Gastaldelli A, Miyazaki Y, Matsuda M, Pettiti M,Natali A, Mari A, De Fronzo RA. Predominant role of reduced beta-cell sensitivity to glucose over insulin resistance in impaired glucose tolerance. Diabetologia,2003; 46: 1211–19.
  8. Hanefeld M, Koehler C, Fuecker K, Henkel E, Schaper F, Temelkova-Kurktschiev T. Insulin secretion and insulin sensitivity pattern is different in isolated impaired glucose tolerance and impaired fasting glucose. Diabetes Care, 2003; 26:868-74.
  9. Abdul-Ghani MA, Tripathy D, DeFronzo RA. Contributions of β-Cell Dysfunction and Insulin Resistance to the Pathogenesis of Impaired Glucose Tolerance and Impaired Fasting Glucose.Diabetes Care, 2006;29: 1130–39.
  10. Song J, Hu X, Riazi S, Tiwari S, Wade JB, Ecelbarguer CA. Regulation of blood pressure, the epithelial sodium channel (ENaC), and other key renal sodium transporters by chronic insulin infusion in rats. Am JPhysiol Renal Physiol, 2006; 290: F1055-64.
  11. Féraille E, Carranza ML, Rousselot M, Favre H. Insulinenhancessodiumsensitivity of Na-K-ATPase in isolated rat proximal convoluted tubule. Am J Physiol, 1994; 267: F55–62.
  12. Gesek F, Schoolwerth A. Insulin increases Na(+)-H+ exchange activity in proximal tubules from normotensive and hypertensive rats. Am J Physiol, 1991; 260: F695–703.
  13. Ito O, Kondo Y, Takahashi N, Kudo K, Igarashi Y, Omata K, Imai Y, Abe K. InsulinstimulatesNaCltransport in isolatedperfused MTAL of Henle’s loop of rabbit kidney. Am J Physiol, 1994; 267: F265–70
  14. Blazer-Yost BL, Liu X, Helman SI. Hormonal regulation of ENaCs: insulin and aldosterone. Am J PhysiolCellPhysiol, 1998; 274: C1373–79.
  15. Raij L.Nitric oxide and thekidney.Circulation, 1993; 87Suppl V: V26-29.
  16. Blazer-Yost BL, Esterman MA, Vlahos CJ. Insulin-stimulated trafficking of ENaC in renal cells requires PI 3-kinase activity. Am J PhysiolCellPhysiol, 2003; 284: C1645–53.
  17. Fuster DG, Bobulescu IA, Zhang J, Wade J, Moe OW. Characterization of theregulation of renal Na+/H+ exchanger NHE3 by insulin. Am J Physiol Renal Physiol, 1997; 292: F577-F585.
  18. Ito O, Kondo Y, Oba M, Takahashi N, Omata K, Abe K. Tyrosinekinase, phosphatidylinositol 3-kinase, and proteinkinase C regulateinsulin-stimulatedNaClabsorption in thethickascendinglimb. KidneyInt, 1997; 51: 1037-41
  19. Zeng G,Nystrom FH, Ravichandran LV, Cong LN, Kirby M, Mostowsky H, Quon MJ. Roles forinsulin receptor, PI3-kinase and Akt in insulin signaling pathways related to production of nitric oxide in human vascular endothelial cells. Circulation, 2000; 101: 1539-45.
  20. Soto C, Juárez J, Pérez J, González I, Esquivel A, Uria E, Pérez S,Raya L. Insulin gene expression and its detection in the rat kidney. Int. Jour. Sci. Res. Tech, 2014; 3: 194-200.
  21. Goren H, Kulkarni R, Kahn C. Glucose homeostasis and tissue transcript content of insulin signaling intermediates in four inbred strains of mice: C57BL/6, C57BLKS/6, DBA/2, and 129X1. Endocrinology, 2004; 145: 3307-23.
  22. Baner C. Chemical Laboratory Methods. New York 7 Academic Press, 1985.
  23. Nakamura R, Emmanouel DS, Katz AI. Insulin binding sites in various segments of the rabbit nephron. J ClinInvest, 1983; 72: 388–92.
  24. Vaziri ND. Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences. Am J Physiol Renal Physio, 2006; 290: F262-72.
  25. Locatelli F., Pozzoni P., Del Vecchio L. 2006. Renal manifestations in the metabolic syndrome. J Am SocNephrol. 17: S81–S85.
  26. Klisic J, Hu MC, Nief V, Reyes L, Fuster D, Moe OW, Ambul PM. Insulin activates Na+/H+ exchanger 3: biphasic response and glucocorticoid dependence. Am J Physiol. Renal Physiol,2002; 283: F532-9.
  27. Takahashi N, Ito O, Abe K. Tubular effects of insulin. Hypertens Res,1996; 19: S41-5
  28. Féraille E., Rousselot M., Rajerison R., Favre H. Effect of insulin on Na+,K+-ATPase in rat collecting duct. JPhysiol, 1995; 488: 171-80.
  29. Blazer-Yost BL, Esterman MA, Vlahos CJ. Insulin-stimulated trafficking of ENaC in renal cells requires PI 3-kinase activity Am J PhysiolCellPhysiol, 2003; 284: C1645-53.
  30. Pearce D. The role of SGK1 in hormone-regulated sodium transport. TrendsEndocrinolMetab, 2001; 12: 341-7.
  31. Zhang YH, de la Rosa DA, Canessa CM, Hayslett JP. Insulin-induced phosphorylation of ENaC correlates with increased sodium channel function in A6 cells. Am J Physiol Cell Physiol, 2005; 288: C141-7.
  32. Tiwari S, Halagappa VK, Riazi S, Hu X, Ecelbarguer CA. Reduced expression of insulin receptors in the kidneys on insulin-resistant rats. J AmSocNephrol, 2007; 18: 2661-71
  33. Tiwari S, Riazi S, Ecelbarguer CA. Insulin’s impact on renal sodium transport and blood pressure in health, obesity, and diabetes. Am JPhysiol Renal Physiol, 2007; 293: F974-84
  34. Bickel CA, Knepper MA, VerbalisJG, Ecelbarger CA. Dysregulation of renal salt and water transport proteins in diabetic Zucker rats. Kidney Int, 2002; 61: 2099-110.
  35. Montagnani M, Ravichandran LV, Chen H, Esposito DL, Quon MJ. Insulin receptor substrate-1 and phosphoinositide-dependent kinase-1 are required for insulin-stimulated production of nitric oxide in endothelial cells. MolEndocrinol,2002; 16: 1931-42.
  36. Knight SF, Imig JD.Obesity, insulin resistance, and renal function. Microcirculation, 2007; 14: 349-62.
  37. Mimram J. Nitric oxide inhibition and renal alterations. J. Cardiovasc. Pharmacol,2001;38 (Suppl 2): S65-S70.
  38. Fujiwara H, Narimatsu Y, Hashimoto S, Hiramatsu K.Angiography of occlusive vascular disease.NihonRinsho, 1999; 57:1526-30.
  39. Hayashi K, Kanda T, Homma K, Tokuyama H, Okubo K, Takamatsu I, Tatematsu S, Kumagai H, Saruta T. Altered renal microvascular response in Zucker obese rats. MetabClinExp, 2002; 51: 1553-61.
  40. Kim JS, Choi KC, Jeong MH, Kim SW, Oh YW, Lee JU. Increased expression of sodium transporters in rats chronically inhibited of nitric oxide synthesis. J Korean Med Sci,2006; 21: 1-4.
  41. Zhu M, Hu J, Perez E, Phillips D, Kim W, Ghaedian R, Napora JK, Zou S. Effects of long-term cranberry supplementation on endocrine pancreas in aging rats. J. Gerontol. A BiolSci MedSci, 2011; 66: 1139–51.
  42. Ihm SH, Moon HJ, Kang JG, Park CY, Oh KW, Jeong IK Oh YS, and Park SW. Effect of aging on insulin secretory function and expression of beta cell function-related genes of islets. Diabetes Res ClinPract, 2007;77 (Suppl 1): S150–4.
  43. Kaneto H, Matsuoka TA, Nakatani Y, Kawamori D, Miyatsuka T, Matsuhisa M., Yamasaki, Y. Oxidative stress, ER stress, and the JNK pathway in type 2 diabetes. J MolMed,2005; 83: 429–39.
  44. Kjørholt C, Akerfeldt MC, BidenTJ, Laybutt DR. Chronic hyperglycemia, independent of plasma lipid levels, is sufficient for the loss of beta-cell differentiation and secretory function in the db/db mouse model of diabetes. Diabetes, 2005; 54: 2755–63.
  45. Szoke E, Shrayyef MZ, Messing S, Woerle HJ, Van Haeften TW, Meyer C, Mitrakou A, Pimenta W, Gerich, JE. Effect of agingon glucose homeostasis: accelerated deterioration of beta-cell function in individuals with impaired glucose tolerance. Diabetes Care,2008; 31: 539–43.
  46. Chang AM and Halter JB. Ageing and insulinsecretion. Am J PhysiolEndocrinolMetab, 2003; 284: E7–12.
  47. DeFronzo RA. Glucose intolerance and aging. Diabetes Care, 1981; 4: 493–501.
  48. Kim DH, KimJM, Lee EK, Choi YJ, Kim CH, Choi JS, Deuk NK, Yu BP, Chung HJ. Modulation of Foxo1 phosphorylation/acetylationbybaicalinduringaging. J. NutrBiochem, 2012; 23: 1277–84.
  49. Silva E, Gomes P, Soares-da-Silva P. Overexpression of Na+/K+-ATPaseparallels the increase in sodium transport and potassium recycling in an in vitro model of proximal tubular celular ageing. JMembraneBiol,2006; 212: 163-75.
  50. Baylis C.Sexualdimorphism in theaging kidney: differences en the nitric oxide system. NatRevNephrol, 2009; 5:384-96.
  51. Roczniakand A, Burns KD. Nitric oxide stimulatesguanylatecyclase and regulatessodium transport in rabbit proximal tubule. Am JPhysiol, 1996; 270: F106-15.
  52. McKee M, Scavone C, Nathanson JA. Nitric oxide, cGMP, and hormone regulation of active sodium transport. ProcNatlAcadSci,1994; 91: 12056-60.
To cite this article

Claudia Soto,JesúsJuárez, Imelda González, Esther Uría,Luis Raya, Mónica Ruiz, Natalia García , " Insulin Gene Expression And Its Detection In The Kidneys Of Rats With Impaired Glucose Tolerance ", International Journal of Latest Research in Science and Technology . Vol. 4, Issue 2, pp 171-179 , 2015

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