Department of Food Science and Nutrition, University of Ulsan, Ulsan, South Korea.
Obesity (Silver Spring). 2010 Apr;18(4):780-7. doi: 10.1038/oby.2009.301. Epub 2009 Oct 1.
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)-alpha, and PPARgamma coactivator-1alpha (PGC-1alpha) mRNAs were also measured by RT-PCR, and PPARalpha 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-alpha (TNFalpha), 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 PPARalpha/PGC-1alpha mRNA in the liver increased. Moreover, luciferase assays revealed that capsaicin is capable of binding PPARalpha. 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 PPARalpha and TRPV-1 expression/activation.
肥胖引起的炎症会导致肥胖相关代谢紊乱的发生，如胰岛素抵抗、2 型糖尿病、脂肪肝和心血管疾病。在这项研究中，我们研究了饮食中的辣椒素是否可以减轻肥胖引起的炎症以及胰岛素抵抗和肝脂肪变性等代谢紊乱。10 周高脂饮食喂养的雄性 C57BL/6 肥胖小鼠再补充 0.015%辣椒素 10 周，并与未补充的对照组进行比较。葡萄糖耐量试验估计葡萄糖耐量。通过逆转录-PCR 和酶联免疫吸附试验测量脂肪细胞因子基因的转录物和相应的蛋白质，通过流式细胞术分析确定巨噬细胞数量。通过 RT-PCR 还测量瞬时受体电位香草酸类型-1（TRPV-1）、过氧化物酶体增殖物激活受体（PPAR）-α 和过氧化物酶体增殖物激活受体γ共激活因子-1α（PGC-1α）mRNA，并进行 PPARα 荧光素酶测定。饮食中的辣椒素降低了空腹血糖、胰岛素、瘦素水平，并显著改善了肥胖小鼠的葡萄糖耐量受损。脂肪组织和肝脏中肿瘤坏死因子-α（TNF-α）、单核细胞趋化蛋白-1（MCP-1）和白细胞介素（IL）-6mRNA 和蛋白质水平显著降低，巨噬细胞浸润、肝甘油三酯和脂肪组织中 TRPV-1 表达也显著降低。同时，脂肪组织中的脂联素 mRNA/蛋白和肝脏中的 PPARα/PGC-1α mRNA 增加。此外，荧光素酶测定表明辣椒素能够结合 PPARα。我们的数据表明，饮食中的辣椒素通过抑制炎症反应以及增强脂肪组织和/或肝脏中的脂肪酸氧化，可能减轻肥胖引起的葡萄糖不耐受，这两者都是影响胰岛素抵抗的重要外周组织。辣椒素在脂肪组织和肝脏中的作用与其对 PPARα 和 TRPV-1 表达/激活的双重作用有关。
