- 发酵姜黄对高脂饮食诱导肥胖小鼠代谢失调和肠道微生物群的调节作用。
Modulatory Effects of -Fermented Turmeric on Metabolic Dysregulation and Gut Microbiota in High-Fat Diet-Induced Obesity in Mice.
机构信息
Department of Food Science, National Quemoy University, Quemoy 89250, Taiwan.
Institute of Food Science and Technology, National Taiwan University, Taipei 10617, Taiwan.
出版信息
J Agric Food Chem. 2024 Aug 14;72(32):17924-17937. doi: 10.1021/acs.jafc.4c01501. Epub 2024 Jul 4.
Turmeric, derived from , and , a lactic acid bacteria, have been studied for their potential antiobesity effects. To date, the antiobesity effects of turmeric fermented with have not been sufficiently investigated. This study was conducted oral administration of 5% fermented (FT) and unfermented turmeric (UT) in diet over 16 weeks using high-fat diet (HFD)-induced obese C57BL/6J mice. Results showed that the curcuminoid content of turmeric decreased following fermentation. Furthermore, FT significantly suppressed weight gain and liver and visceral adipose tissue weight and reduced plasma metabolic parameters in both the UT and FT experimental groups. The effects of FT were more noticeable than those of the unfermented form. Moreover, FT downregulated the expression of adipogenesis, lipogenesis, and inflammatory-related protein, but upregulated liver β-oxidation protein SIRT 1, PPARα, and PGC-1α in perigonadal adipose tissue. Additionally, FT ameliorated insulin resistance by activating insulin receptor pathway protein expressions in visceral adipose tissues. FT also modulated gut microbiota composition, particularly in two beneficial bacteria, and as well as two short-chain fatty acid-producing bacteria: and . Our findings indicate that the modulation effect of FT may be an important pathway for its antiobesity mechanisms.
姜黄,来源于 和 ,是一种乳酸菌,其潜在的抗肥胖作用已被研究。迄今为止,用 发酵的姜黄的抗肥胖作用尚未得到充分研究。本研究采用高脂肪饮食(HFD)诱导的肥胖 C57BL/6J 小鼠,通过口服 5%发酵(FT)和未发酵姜黄(UT)16 周,进行了研究。结果表明,发酵后姜黄中的姜黄素含量降低。此外,FT 显著抑制体重增加以及肝和内脏脂肪组织重量,并降低 UT 和 FT 实验组的血浆代谢参数。FT 的作用比未发酵形式更为明显。此外,FT 通过下调围性腺脂肪组织中脂肪生成、脂生成和炎症相关蛋白的表达,而上调肝脏β-氧化蛋白 SIRT1、PPARα 和 PGC-1α 的表达,来改善胰岛素抵抗。FT 还通过激活内脏脂肪组织中胰岛素受体通路蛋白的表达来调节肠道微生物群组成,特别是两种有益细菌 和 以及两种产生短链脂肪酸的细菌 和 。我们的研究结果表明,FT 的调节作用可能是其抗肥胖机制的重要途径。