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Naringin (30 mg/kg) and vitamin C (50 mg/kg) cotreatment ameliorated streptozotocin-induced diabetes in rats by improving insulin concentration and prevented oxidative stress. It also improved insulin concentration and pancreatic architecture in db/db mice at a supplementation dose of 0.2 g/kg of diet. Alteration of glucose-regulating enzyme activities also plays a crucial role in the glucose-lowering effect of naringin in experimental animals. Naringin markedly lowered the activity of hepatic glucose-6-phosphatase and phosphoenolpyruvate carboxy kinase in db/db mice compared with control mice. Recent investigations also suggested that the hypoglycemic activity of naringin is mediated via uptake of glucose in the skeletal muscle. Maximum stimulation was seen with 75 μmol/L naringenin for 2 h, which was comparable to maximum insulin response in L6 myotubes. Increased glucose uptake is mediated via upregulation of AMPK in skeletal muscle cells. AMPK-activated improvement in metabolic syndrome was also reported by Pu et al. In this study, naringin supplementation (0.2 g/kg of diet) improved glucose intolerance and insulin resistance in a model of high-fat-diet–fed mice.
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