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在脂肪肝形成前补充木犀草素可通过抑制内脏脂肪组织脂解改善肥胖小鼠的肝脂肪变性。

Diet Supplementation of Luteolin before Fatty Liver Formation Improves Hepatic Steatosis in Obese Mice by Inhibiting Visceral Adipose Tissue Lipolysis.

作者信息

Wang Jiahui, Zhang Zhixin, Lin Yan, Chen Juan, Wang Fangbin, Wang Lu, Liu Jian, Zhang Xian

机构信息

School of Food and Biological Engineering, Hefei University of Technology, Hefei, Anhui, 230009, China.

Engineering Research Center of Bioprocess, Ministry of Education, Hefei University of Technology, Hefei, Anhui, 230009, China.

出版信息

Mol Nutr Food Res. 2023 Apr;67(7):e2200478. doi: 10.1002/mnfr.202200478. Epub 2023 Mar 17.

DOI:10.1002/mnfr.202200478
PMID:36760156
Abstract

SCOPE

Serotonin (5-HT)-induced visceral adipocyte lipolysis is essential for the development of obesity-related complications. Diet supplementation of luteolin prevents high-fat diet (HFD)-fed mice against obesity and associated fatty liver. However, independent of the body weight loss, whether dietary luteolin can substantially reduce hepatic steatosis remains unclear.

METHODS AND RESULTS

In differentiated 3T3-L1 cells, 5-HT treatment promotes adipocyte lipolysis, while luteolin significantly inhibits 5-HT-induced lipolysis, Ca -PKG cascade, and SIRT1/FoxO1/AMPKα signaling through binding to 5-HT receptor HTR2B. Further, 5-week-old mice are fed with an HFD for 16 weeks. At the 6th, 8th, or 10th weeks of HFD feeding, some mice are switched to a luteolin-containing HFD, respectively. In all HFD-fed mice, body weight gain and body component are unaffected by dietary luteolin. However, diet supplementation of luteolin at the 6th or 8th, rather than at the 10th weeks, alleviates hepatic steatosis. Meanwhile, dietary luteolin reduces epididymal adipose tissue (EAT) lipolysis, and represses the level of lipolytic enzyme, the expression of Htr2b, and the activation of PKG and SIRT1/FoxO1/AMPKα signaling in EAT.

CONCLUSIONS

Diet supplementation of luteolin before the formation of fatty liver protects HFD-fed mice against ectopic lipid deposition in liver by inhibiting visceral adipocyte lipolysis.

摘要

范围

血清素(5-羟色胺,5-HT)诱导的内脏脂肪细胞脂解对于肥胖相关并发症的发展至关重要。饮食中添加木犀草素可防止高脂饮食(HFD)喂养的小鼠肥胖及出现相关脂肪肝。然而,独立于体重减轻之外,饮食中的木犀草素是否能显著降低肝脂肪变性尚不清楚。

方法与结果

在分化的3T3-L1细胞中,5-HT处理可促进脂肪细胞脂解,而木犀草素通过与5-HT受体HTR2B结合,显著抑制5-HT诱导的脂解、Ca-PKG级联反应以及SIRT1/FoxO1/AMPKα信号通路。此外,给5周龄小鼠喂食HFD 16周。在HFD喂养的第6、8或10周,分别将部分小鼠换成含木犀草素的HFD。在所有HFD喂养的小鼠中,饮食中的木犀草素不影响体重增加和身体成分。然而,在第6周或第8周而非第10周饮食中添加木犀草素可减轻肝脂肪变性。同时,饮食中的木犀草素可减少附睾脂肪组织(EAT)的脂解,并抑制EAT中脂解酶水平、Htr2b的表达以及PKG和SIRT1/FoxO1/AMPKα信号通路的激活。

结论

在脂肪肝形成之前饮食中添加木犀草素可通过抑制内脏脂肪细胞脂解,保护HFD喂养的小鼠肝脏免受异位脂质沉积。

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