Antidiabetic Effect of Vitamin D3 and /or Metformin on Type 2 induced Diabetes in Male Rats

Metabolic syndrome (MS) is manifested as a cluster of ailments that Encompass central obesity, insulin resistance, compromised glucose tolerance, and high blood pressure. The purpose of our study was to examine the role of vitamin D3 and/or metformin administration in ameliorating Glucose, insulin, Homa IR, oxidative indicators, and inflammatory markers in type 2 diabetes mellitus (T2DM). Fifty male Sprague-Dawley rats were randomly assigned to five groups, including ten rats in each, as follows: Group one: control, Group two: diabetic group received a single sub-diabetogenic dose of streptozotocin (STZ) (35 mg/kg BW intraperitoneal and high fat high fructose diet (HFHF/S). Group Three: diabetic group treated with vitamin D3 by dose (10μg/kg/day), Group Four: diabetic group treated with metformin (250 mg/kg/day). Group five: diabetic group treated with vitamin D3 and metformin. Rats were sacrificed. Furthermore investigations were done. Data showed that oral administration of vitamin D3 orally reversed HFHF-mediated alterations by lowering the serum glucose, insulin, triglycerides (TAG), total cholesterol (TC), LDL-cholesterol (LDL-c), VLDL-cholesterol (VLDL-c), as well as reducing of HOMA-IR., Also, a significant heigh levels of serum HDL-c. Decrease level of malondialdehyde (MDA). On another hand increase level of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) and decrease level of tumor necrosis factor (TNF-α), interleukin 6 (IL6) and leptin while increase in adiponectin and ghrelin, also vitamin D3 induced a downregulation of mRNA levels for peroxisome proliferator-activated receptor γ (PPARγ), sterol regulatory element binding protein (SREBP-1c), smoothened (SMO), protein patched homolog 1 (PTCH-1), and GLI in liver and adipose tissues. Additionally, it led to the upregulation of Farnesoid X receptor (FXR) mRNA levels in liver tissue. Vitamin D3 emerges as a promising candidate for managing metabolic syndrome and warrants further investigation into its underlying mechanisms