Volume 7, Issue 2 (Vol.7 No.2 Jan 2019)                   rbmb.net 2019, 7(2): 217-222 | Back to browse issues page

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Derakhshanian H, Djazayery3 A, Javanbakht M H, Eshraghian M R, Mirshafiey A, Zarei M, et al . The Effect of Vitamin D on Cellular Pathways of Diabetic Nephropathy. rbmb.net. 2019; 7 (2) :217-222
URL: http://rbmb.net/article-1-204-en.html
Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.
Abstract:   (284 Views)
Background: Diabetic nephropathy is one of the most important microvascular complications and a major cause of morbidity and mortality in diabetic patients. This study was designed to investigate the effect of vitamin D on the expression of three key genes involved in the development of diabetic nephropathy.

Methods: Twenty-four male Sprague–Dawley rats were randomly divided into three groups. The first group served as control and the other two groups received intraperitoneal injections of 45 mg/kg STZ to develop diabetes. The groups were treated for four weeks either with placebo or two vitamin D injections of 20,000 IU/kg. Serum glucose, insulin, and HbA1c levels, and AGE cellular receptor (RAGE), aldose reductase (AR) and glutamine: fructose-6-phosphate aminotransferase (GFAT) gene expression were assessed in kidney tissue at the end of the experiment.

Results: Vitamin D treatment resulted in a significant increase in insulin concentration, which could improve hyperglycaemia in diabetic rats. Serum HbA1c decreased slightly but insignificantly following the vitamin D injections. In addition, expression of GFAT, a key regulatory enzyme in the hexosamine pathway, was significantly reduced following vitamin D administration.

Conclusions: Vitamin D may reduce diabetic nephropathy not only by improving blood glucose and insulin levels, but also by modulating hexosamine pathways in kidney.
Full-Text [PDF 629 kb]   (188 Downloads)    
Type of Article: Original Article | Subject: Molecular Biology
Received: 2017/10/24 | Accepted: 2017/12/14

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