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Valproic Acid Improves Glucose Homeostasis by Increasing Beta‐Cell Proliferation, Function, and Reducing its Apoptosis through HDAC Inhibition in Juvenile Diabetic Rat
Author(s) -
Khan Sabbir,
Jena Gopabandhu
Publication year - 2016
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21807
Subject(s) - apoptosis , valproic acid , beta cell , diabetes mellitus , cell growth , endocrinology , streptozotocin , medicine , beta (programming language) , glucose homeostasis , cell , biology , chemistry , pharmacology , insulin resistance , biochemistry , islet , neuroscience , computer science , programming language , epilepsy
Recent evidence highlighted that there is a link between type‐1 diabetes mellitus and histone deacetylases (HDACs) due to their involvement in beta‐cell differentiation, proliferation, and function. The present study aimed to investigate the protective role of valproic acid (VPA) on beta‐cell proliferation, function, and apoptosis in juvenile diabetic rat. Diabetes was induced in juvenile Sprague–Dawley rats by streptozotocin (75 mg/kg, i.p.) and VPA was administered at the doses of 150 and 300 mg/kg/day for 3 weeks by oral route. Various biochemical parameters, cellular alterations, and protein expression as well as apoptosis were assessed using different assays. VPA treatment significantly decreased plasma glucose, beta‐cell damage, and apoptosis as well as increased the beta‐cell function, insulin level/expression. The present study demonstrated that VPA improves beta‐cell proliferation and function as well as reduces beta‐cell apoptosis through HDAC inhibition. Our findings provide evidence that VPA may be useful for the treatment of juvenile diabetes.