Ojochenemi Aladi ENEJOH2023-09-222023-09-222021-11-11https://teras.ng/api/asset/document/b8020aa7-0065-47a0-8930-e1361524d954https://teras.ng/catalog-item/2d91ca21-6ea3-4b74-ba9f-8a625216342dhttp://dspace.teras-network.net:4000/handle/123456789/23948The results showed that CoF up-regulated the expression of insulin and pancreatic duodenal homeobox-1 genes in the pancreas, and GLP-1 in the intestine. In the kidney, BUN/SC levels were restored to pre-STZ treatment states following CoF treatment. Inflammatory and kidney injury molecule -1 genes were equally significantly down-regulated (p<0.05) in STZ-CoF treated group in comparison with STZ-only group. In the aorta, the significant increase of inflammatory genes as a result of STZ treatment, were down-regulated by CoF intervention. CoF also significantly increased antioxidant genes that were down-regulated in the STZ-only group. Histo-structural alterations associated with STZ treatment were completely reversed in STZ-CoF group in the pancreas, kidney and aorta. NOAEL experiments revealed that CoF is relatively safe up to doses of 100 mg/kg b.w. Moleculardynamics simulation confirmed TGR5 as the putative target, where it evolved active state conformation from a starting intermediate state conformation when bound to CoF. Further studies revealed that the performance ofCoF was highly comparable with metformin (an anti-diabetic drug).Undergraduate Theses