Ankaflavin regulates adipocyte function and attenuates hyperglycemia caused by high-fat diet via PPAR-γ activation

Abstract

The effects of ankaflavin (AK) on adipokines level and insulin sensitivity were investigated. Mice were fed with high-fat diet (HFD) and AK to evaluate hyperglycemia and hyperlipidemia. Additionally, mature differentiated 3T3-L1 adipocytes were treated with AK or monascin (MS) to determine insulin signaling. Results showed that AK down-regulated serum and hepatic triacylglyceride (TG) and total cholesterol (TC) levels in mice, ameliorating hyperglycemia and hyperinsulinemia symptoms elicited by the HFD. AK elevated serum adiponectin levels in HFD-induced mice and mature 3T3-L1 adipocytes. The effect of AK on insulin sensitivity and adipokines secretion were abolished by peroxisome proliferator activated receptor-γ PPAR-γ antagonist GW9662. Moreover, we made the novel discovery that AK markedly promoted insulin receptor and Akt phosphorylation, and increased glucose uptake in mature 3T3-L1 adipocytes to a greater extent than did MS. Taken together, AK attenuated insulin resistance in HFD-induced mice and promoted insulin sensitivity in 3T3-L1 adipocytes through PPAR-γ activation.

Keywords

• Ankaflavin
• Peroxisome proliferator activated receptor-γ (PPAR-γ)
• High-fat diet
• GW9662
• Adipokines