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

Wei Hsuan Hsu; Te Han Liao; Bao Hong Lee; Ya Wen Hsu; Tzu Ming Pan

doi:10.1016/j.jff.2012.09.003

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

Wei Hsuan Hsu, Te Han Liao, Bao Hong Lee, Ya Wen Hsu, Tzu Ming Pan

Department of Food Safety / Hygiene and Risk Management

Research output: Contribution to journal › Article › peer-review

23 Citations (Scopus)

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.

Original language	English
Pages (from-to)	124-132
Number of pages	9
Journal	Journal of Functional Foods
Volume	5
Issue number	1
DOIs	https://doi.org/10.1016/j.jff.2012.09.003
Publication status	Published - 2013 Jan

All Science Journal Classification (ASJC) codes

Food Science
Medicine (miscellaneous)
Nutrition and Dietetics

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10.1016/j.jff.2012.09.003

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title = "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.",

author = "Hsu, {Wei Hsuan} and Liao, {Te Han} and Lee, {Bao Hong} and Hsu, {Ya Wen} and Pan, {Tzu Ming}",

note = "Funding Information: The authors would like to express our gratitude to National Science Council, ROC , for supporting this research work ( NSC99-2628-B-002-004-MY2 ) and subsidiary. Copyright: Copyright 2013 Elsevier B.V., All rights reserved.",

year = "2013",

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doi = "10.1016/j.jff.2012.09.003",

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AU - Hsu, Wei Hsuan

AU - Liao, Te Han

AU - Lee, Bao Hong

AU - Hsu, Ya Wen

AU - Pan, Tzu Ming

N1 - Funding Information: The authors would like to express our gratitude to National Science Council, ROC , for supporting this research work ( NSC99-2628-B-002-004-MY2 ) and subsidiary. Copyright: Copyright 2013 Elsevier B.V., All rights reserved.

PY - 2013/1

Y1 - 2013/1

N2 - 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.

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

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