Egyptian Journal of Basic and Applied Sciences · 2017 · 11 citations · 38 references
MedicineEndocrinologyPharmacologyBiochemical PharmacologyHormone BiochemistryMetabolic RegulationAdipose TissueDiabetes MellitusDiabetes Mellitus BiochemistryInsulin ResistanceAdiponectin SignalingAdipose Tissue DysfunctionInsulin ActionOxidative Stress In DiabetesPeroxisome Proliferator-activated Receptor SignalingPeroxisome Proliferator-activated ReceptorsType 2 Diabetes Mellitus PathogenesisType 2 Diabetes Pathophysiology
Type 2 diabetes mellitus (T2DM) is the most common type of diabetes, accounting for 90% of diabetic cases. It is characterized by chronic hyperglycemia which is caused by a combination of deficiency in insulin action and secretion. Adipose tissue regulates insulin sensitivity via the circulating adipocytokines, leptin, resistin and adiponectin. Hypoadiponectinemia contributes to the development of obesity and related disorders such as diabetes, hyperlipidemia and cardiovascular diseases. The present study aimed to evaluate the beneficial effect of flavonoid 2-hydroxychalcone in T2DM through its effect on peroxisome proliferator activated receptor gamma (PPAR-γ) and adiponectin. T2DM was induced in male Wistar rats using high fat diet and low dose of streptozotocin (STZ, 35 mg/kg, i.p.). The flavonoid 2-hydroxychalcone was administered by oral tubes. Levels of PPAR-γ in sub abdominal adipose tissue, serum adiponectin, serum tumor necrosis factor-α (TNF-α) and serum insulin levels were detected by ELISA. Moreover, malondialdehyde (MDA) and reduced glutathione (GSH) in sub abdominal adipose tissue, fasting serum glucose, serum triglycerides and serum total cholesterol levels were measured by colorimetric methods. Results showed that 2-hydroxychalcone attenuated changes induced by T2DM in rats. 2-Hydroxychalcone treatment increased PPAR-γ levels in adipose tissue, reduced oxidative stress, restored adiponectin levels and decreased high glucose levels in T2DM rats. In conclusion, 2-hydroxychalcone reduced hyperglycemia in T2DM by regulating adiponectin secretion. This effect involves PPAR-γ signaling pathway.
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