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Effect of Naringin on Hyperglycemia and Diabetes

Hyperglycemia and insulin resistance are common features of metabolic syndrome. Insulin resistance can be defined as decreased response of the peripheral tissues to insulin action. Certain inflammatory cytokine such as TNF-α may cause insulin resistance in experimental models of obesity. Moreover, several studies showed that IL-6 and TNF-α concentrations were increased in individuals with insulin resistance and type 2 diabetes. On the other hand, inflammatory cytokines such as TNF-α and IL-6 may also cause dysfunction of peripheral insulin receptor and insulin resistance and ultimately increase glucose concentrations in plasma. A high-fat diet increased inflammatory cytokines and caused insulin resistance and hyperglycemia. The hypoglycemic effect of naringin is well documented.

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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