Activating the AMPK by DHPO to Mitigate Lipid Abnormalities and Insulin
Journal Title: Saudi Journal of Medicine - Year 2017, Vol 2, Issue 3
Abstract
Abstract: Metabolic syndrome such as type-2 diabetes and obesity is becoming formidable health issue around the world. This study demonstrate the effect of a small molecule 2-(3,4-dihydro-2H-pyrrolium-1-yl)-3oxoindan-1-olate (DHPO), on metabolic syndrome diet induce obese rats(8-9 weeks old) . Rats were divided into three groups, Two groups were fed either a corn starch–rich (C) or high-carbohydrate, high-fat (H) diet for 16 weeks, the third group (HD) was fed high-carbohydrate, high-fat diet, for the first 8 weeks and the diet was supplemented with DHPO (0.4 g/kg food) for a additional 8 weeks. H and C diets contained 68% carbohydrates, as fructose and sucrose in H diet and as polysaccharides in C diet, and C diet contained 24 and 0.7% fat. The high-carbohydrate, high-fat diet produced obesity, hypertension, dyslipidaemia, impaired glucose tolerance, NAFLD, cardiovascular remodelling, and endothelial dysfunction. DHPO promote glucose disposal and corrected dyslipidaemia in dietary rats (high-carbohydrate, high-fat) by enhanced insulin signalling pathway such as AMPK. In addition, DHPO augmented glucose-uptake in gastrocnemius muscles. Therefore, DHPO may be the novel component that improve endothelial dysfunction and impaired glucose tolerance which cause type-2 diabetes. Keywords: AMPK, DHPO, lipid abnormalities, insulinresistance
Authors and Affiliations
Aboajela Ramadan Imbark Ajaj, Ashraf Mohamed Albakoush, AzabElsayed Azab
Keywords
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