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膳食山奈酚通过AMPK/SIRT1/PGC-1α信号通路诱导白色脂肪细胞褐变,从而发挥抗肥胖作用。

Dietary kaempferol exerts anti-obesity effects by inducing the browing of white adipocytes via the AMPK/SIRT1/PGC-1α signaling pathway.

作者信息

Xu Changyu, Zhang Xiaoxi, Wang Yihuan, Wang Yan, Zhou Yixuan, Li Fenfen, Hou Xiaoli, Xia Daozong

机构信息

Department of Food Science and Nutrition, School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Academy of Chinese Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

出版信息

Curr Res Food Sci. 2024 Mar 28;8:100728. doi: 10.1016/j.crfs.2024.100728. eCollection 2024.

DOI:10.1016/j.crfs.2024.100728
PMID:38577419
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10990952/
Abstract

Browning of white adipose tissue is a novel approach for the management of obesity and obesity-related metabolic disorders. Kaempferol (KPF) is a common dietary nutrient found abundantly in many fruits and vegetables and has been shown to have the potential to regulate lipid metabolism. However, the detailed mechanism by which it affects the browning of white adipose tissue remains unclear. In the present study, we sought to determine how KPF induces adipocytes to undergo a browning transformation by establishing a primary adipocyte model and an obese mouse model. Our results showed that KPF-treated mice were rescued from diet-induced obesity, glucose tolerance and insulin resistance, associated with increased expression of adaptive thermogenesis-related proteins. KPF-promoted white adipose browning correlated with the AMPK/SIRT1/PGC-1α pathway, as the use of an AMPK inhibitor in preadipocytes partially reversed the observed browning phenotype of KPF-treated cells. Taken together, these data suggest that KPF promotes browning of white adipose tissue through activation of the AMPK/SIRT1/PGC-1α pathway. This study demonstrates that KPF is a promising natural product for the treatment of obesity by promoting white fat browning.

摘要

白色脂肪组织的褐变是治疗肥胖及肥胖相关代谢紊乱的一种新方法。山奈酚(KPF)是一种常见的膳食营养素,在许多水果和蔬菜中大量存在,并且已显示出具有调节脂质代谢的潜力。然而,其影响白色脂肪组织褐变的详细机制仍不清楚。在本研究中,我们试图通过建立原代脂肪细胞模型和肥胖小鼠模型来确定KPF如何诱导脂肪细胞发生褐变转化。我们的结果表明,用KPF处理的小鼠从饮食诱导的肥胖、葡萄糖耐量和胰岛素抵抗中得到缓解,这与适应性产热相关蛋白表达增加有关。KPF促进的白色脂肪褐变与AMPK/SIRT1/PGC-1α途径相关,因为在前脂肪细胞中使用AMPK抑制剂部分逆转了KPF处理细胞所观察到的褐变表型。综上所述,这些数据表明KPF通过激活AMPK/SIRT1/PGC-1α途径促进白色脂肪组织的褐变。本研究表明,KPF是一种有前景的天然产物,可通过促进白色脂肪褐变来治疗肥胖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/8dec6c16c634/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/9b532a9f3a0f/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/136fd72a3774/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/6c95fac92b96/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/15580b2bd80b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/619906f13206/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/8dec6c16c634/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/9b532a9f3a0f/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/136fd72a3774/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/6c95fac92b96/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/15580b2bd80b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/619906f13206/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0002/10990952/8dec6c16c634/gr5.jpg

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