NTU568 紅麴菌株研究成果 -- Ankaflavin Regulates Adipocyte Function and Attenuates Hyperglycemia Caused by High-Fat Diet via PPAR-g Activation
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Ankaflavin Regulates Adipocyte Function and Attenuates Hyperglycemia Caused by High-Fat Diet via PPAR-g Activation    HOME > Research Achievement > Publication of monascin and ankaflavin > Improves blood lipids and prevents obesity

Ankaflavin Regulates Adipocyte Function and Attenuates Hyperglycemia Caused by High-Fat Diet via PPAR-g Activation

J Funct Foods (2013) 5: 124-132

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 oninsulin sensitivity and adipokines secretion were abolished by peroxisome proliferatoractivated receptor-gamma 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.

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