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Updated: Jan 23, 2026

Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer
Published on: October 10, 2012
Vitamin D suppresses cellular pathways of diabetes complication in liver
Hoda Derakhshanian1,2, Mahmoud Djalali3, Mohammad Hassan Mohammad Hassan3
1Dietary Supplements and Probiotic Research Center, Alborz University of Medical Sciences, Karaj, Iran.
Objectives:
The aim of this study was to investigate the effect of vitamin D on glucose metabolism, as well as the expression of five key genes involved in the development of diabetes complications in liver tissue of diabetic rats.
Materials And Methods:
Twenty-four male Sprague-Dawley rats were randomly divided into three groups (8 rats in each group). The first group served as control and the other two groups received an intraperitoneal injection of 45 mg/kg streptozotocin to develop diabetes. Groups were treated for four weeks either with placebo or vitamin D (two injections of 20000 IU/kg). Thereafter, serum levels of glucose, insulin and HbA1c were assessed. Liver tissue was examined for the level of advanced glycation end products (AGEs) and the gene expression of AGE cellular receptor (AGER), glyoxalase-1 (GLO-1), aldose reductase (AR), O-linked N-acetylglucosamine transferase (OGT) and glutamine/ fructose-6-phosphate aminotransferase (GFAT).
Results:
Vitamin D injection resulted in a significant increase in plasma level of 25-hydroxycholecalciferol, which could improve hyperglycemia about 11% compared to placebo-receiving diabetic rats (P=0.005). Insulin level increased as a result of vitamin D treatment compared to control (3.31±0.65 vs. 2.15±0.79; P= 0.01). Serum HbA1c and liver AGE concentrations had a slight but insignificant reduction following vitamin D intake. Moreover, a significant decline was observed in gene expression of AGER and OGT in liver tissue (P=0.04 and P<0.001 respectively).
Conclusion:
Vitamin D might contribute in ameliorating diabetes complications not only by improving blood glucose and insulin levels, but also by suppressing AGER and OGT gene expression in the liver.
Insights
Vitamin D supplementation improved hyperglycemia and insulin levels in diabetic rats. It also reduced the expression of specific genes linked to diabetes complications in the liver.
Area of Science:
- Endocrinology and Metabolism
- Molecular Biology
- Nutritional Science
Background:
- Diabetes complications arise from complex metabolic dysregulation.
- Key genes in the liver play a crucial role in the pathogenesis of diabetic complications.
- Vitamin D's role in glucose metabolism and its impact on diabetes-related gene expression require further investigation.
Purpose of the Study:
- To evaluate the effect of vitamin D on glucose metabolism in diabetic rats.
- To assess the impact of vitamin D on the expression of five key genes involved in diabetes complications within liver tissue.
Main Methods:
- Diabetic rat model induced by streptozotocin.
- Treatment groups received either placebo or vitamin D for four weeks.
- Assessed serum glucose, insulin, HbA1c, liver advanced glycation end products (AGEs), and gene expression of AGER, GLO-1, AR, OGT, and GFAT.
Main Results:
- Vitamin D treatment significantly increased 25-hydroxycholecalciferol levels and improved hyperglycemia by 11%.
- Insulin levels were significantly increased in vitamin D-treated rats compared to controls.
- A significant reduction in the gene expression of AGE cellular receptor (AGER) and O-linked N-acetylglucosamine transferase (OGT) was observed in the liver.
Conclusions:
- Vitamin D may help ameliorate diabetes complications by improving glycemic control and insulin levels.
- Vitamin D supplementation demonstrated a suppressive effect on AGER and OGT gene expression in the liver of diabetic rats.
- These findings suggest a potential therapeutic role for vitamin D in managing diabetes and its associated complications.
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