Department of Food and Nutrition, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-749, Republic of Korea.
Food Chem. 2013 Dec 15;141(4):3627-35. doi: 10.1016/j.foodchem.2013.06.028. Epub 2013 Jun 17.
This study examined the effect of piperine on hepatic steatosis and insulin resistance induced in mice by feeding a high-fat diet (HFD) for 13 weeks and elucidated potential underlying molecular mechanisms. Administration of piperine (50 mg/kg body weight) to mice with HFD-induced hepatic steatosis resulted in a significant increase in plasma adiponectin levels. Also, elevated plasma concentrations of insulin and glucose and hepatic lipid levels induced by feeding a HFD were reversed in mice when they were administered piperine. However, piperine did not reduce body weight and other biochemical markers to an extent where they became equal to the levels found in the CD-fed mice. Piperine reversed HFD-induced down-regulation of adiponecitn-AMP-activated protein kinase (AMPK) signalling molecules which play an important role in mediating lipogenesis, fatty acid oxidation and insulin signalling in the livers of mice. The expressions of lipogenic target genes were decreased, whereas the expression of carnitine palmitoyltransferase 1 (CPT1) gene involved in fatty acid oxidation was increased in the livers of the Pin50 group. Piperine significantly decreased the phosphorylation of insulin receptor substrate-1 (IRS-1) compared with the HFD-fed mice. Administration of piperine appeared to reverse preexisting HFD-induced hepatic steatosis and insulin resistance, probably by activation of adiponectin-AMPK signalling in mice.
本研究探讨了胡椒碱对高脂肪饮食(HFD)喂养 13 周诱导的小鼠肝脂肪变性和胰岛素抵抗的影响,并阐明了潜在的分子机制。给 HFD 诱导的肝脂肪变性小鼠施用胡椒碱(50mg/kg 体重)可显著增加血浆脂联素水平。此外,当给 HFD 喂养的小鼠施用胡椒碱时,可逆转由 HFD 引起的升高的血浆胰岛素和葡萄糖浓度以及肝脂质水平。然而,胡椒碱并没有将体重和其他生化标志物降低到与 CD 喂养的小鼠相同的水平。胡椒碱逆转了 HFD 诱导的脂联素-AMP 激活蛋白激酶(AMPK)信号分子的下调,这些信号分子在介导肝脏中的脂肪生成、脂肪酸氧化和胰岛素信号中起重要作用。脂生成靶基因的表达减少,而参与脂肪酸氧化的肉毒碱棕榈酰转移酶 1(CPT1)基因的表达在 Pin50 组的肝脏中增加。与 HFD 喂养的小鼠相比,胡椒碱显著降低了胰岛素受体底物-1(IRS-1)的磷酸化。胡椒碱的给药似乎通过激活小鼠的脂联素-AMPK 信号转导来逆转先前存在的 HFD 诱导的肝脂肪变性和胰岛素抵抗。