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Effect of Long-Term Administration of Oral Magnesium Sulfate and Insulin to Reduce Streptozotocin-Induced Hyperglycemia in Rats: The Role of Akt2 and Irs1 Gene Expressions Publisher Pubmed



Kamran M1, 2 ; Kharazmi F1, 3 ; Malekzadeh K3 ; Talebi A4 ; Khosravi F1, 3 ; Soltani N2, 3, 5
Authors
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Authors Affiliations
  1. 1. Physiology Department, Faculty of Medicine, Hormozgan University of Medical Science, Bandar Abbas, Iran
  2. 2. Endocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran
  3. 3. Molecular Medicine Research Center, Hormozgan University of Medical Science, Bandar Abbas, Iran
  4. 4. Clinical Pathology Department, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran
  5. 5. Physiology Department, School of Medicine, Isfahan University of Medical Science, Isfahan, Iran

Source: Biological Trace Element Research Published:2019


Abstract

The effects of long-term oral administration of magnesium sulfate and insulin on hyperglycemia were investigated using Akt2 and IRS1 gene expression methods in streptozotocin-induced diabetic rats. Fifty rats were randomly divided into five experimental groups: 1, non-diabetic control (NDC); 2, Mg2+-treated non-diabetic control (Mg-NDC); 3, chronic diabetic (CD); 4, Mg2+-treated chronic diabetic (Mg-CD); and 5, insulin-treated chronic diabetic (Ins-CD). Streptozotocin was used to induce diabetes. The Mg-CD and Mg-NDC groups received 10 g/l of MgSO4 added to drinking water. The Ins-CD group received 2.5 U/kg of insulin twice a day. Blood glucose level and body weight were measured every week. The intraperitoneal glucose tolerance test (IPGTT) was performed after 16 weeks. MgSO4 administration improved the blood glucose level and IPGTT. It also increased Akt2 and IRS1 genes as well as protein expression. Insulin lowered the blood glucose level and increased IRS1 gene and protein expression, but did not affect Akt2 gene and protein expression. Glucose reduction after Mg therapy may be mediated, at least partially, via IRS1 and Akt2 genes and protein stimulation. In insulin-treated rats, insulin resistance was not significant due to the absence of Akt2 gene expression. © 2018, Springer Science+Business Media, LLC, part of Springer Nature.
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