Dietary Capsaicin Reduces Obesity‐induced Insulin Resistance and Hepatic Steatosis in Obese Mice Fed a High‐fat Diet

Obesity - Tập 18 Số 4 - Trang 780-787 - 2010
Ji‐Hye Kang1, Tsuyoshi Goto2,3, In‐Seob Han4, Teruo Kawada3, Young Min Kim5, Rina Yu1
1Department of Food Science and Nutrition, University of Ulsan, Ulsan, South Korea
2Department of Applied Life Science, Faculty of Applied Biological Sciences, Gifu University, Gifu, Japan
3Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Kyoto, Japan
4Department of Biological Science, Ulsan, South Korea
5Department of Pathology, University of Ulsan College of Medicine, Ulsan, South Korea

Tóm tắt

Obesity‐induced inflammation contributes to the development of obesity‐related metabolic disorders such as insulin resistance, type 2 diabetes, fatty liver disease, and cardiovascular disease. In this study, we investigated whether dietary capsaicin can reduce obesity‐induced inflammation and metabolic disorders such as insulin resistance and hepatic steatosis. Male C57BL/6 obese mice fed a high‐fat diet for 10 weeks received a supplement of 0.015% capsaicin for a further 10 weeks and were compared with unsupplemented controls. Glucose intolerance was estimated by glucose tolerance tests. Transcripts of adipocytokine genes and the corresponding proteins were measured by reverse transcription‐PCR and enzyme‐linked immunosorbent assay, and macrophage numbers were determined by flow cytometric analysis. Transient receptor potential vanilloid type‐1 (TRPV‐1), peroxisome proliferator–activated receptor (PPAR)‐α, and PPARγ coactivator‐1α (PGC‐1α) mRNAs were also measured by RT‐PCR, and PPARα luciferase assays were performed. Dietary capsaicin lowered fasting glucose, insulin, leptin levels, and markedly reduced the impairment of glucose tolerance in obese mice. Levels of tumor necrosis factor‐α (TNFα), monocyte chemoattractant protein‐1 (MCP‐1), and interleukin (IL)‐6 mRNAs and proteins in adipose tissue and liver decreased markedly, as did macrophage infiltration, hepatic triglycerides, and TRPV‐1 expression in adipose tissue. At the same time, the mRNA/protein of adiponectin in the adipose tissue and PPARα/PGC‐1α mRNA in the liver increased. Moreover, luciferase assays revealed that capsaicin is capable of binding PPARα. Our data suggest that dietary capsaicin may reduce obesity‐induced glucose intolerance by not only suppressing inflammatory responses but also enhancing fatty acid oxidation in adipose tissue and/or liver, both of which are important peripheral tissues affecting insulin resistance. The effects of capsaicin in adipose tissue and liver are related to its dual action on PPARα and TRPV‐1 expression/activation.

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Thông tin
Thông tin xuất bản

Obesity

Tập 18 Số 4

780-787

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