Adipose FGF21 signalling mediates the anti-senescence effects of protein restriction.

Xiaohan Yang, Yanni Wu, Yi Yang, Long Huang, Xianyang Jin, Xuemei Jiang, Chao Jin, Bin Feng, Lianqiang Che, Shengyu Xu, Yan Lin, Yong Zhuo, De Wu, Lun Hua

Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, China.Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, China. · pubmed

Paper

Abstract

Dietary protein restriction (PR) is a well-recognized nutritional intervention that enhances metabolic health and extends lifespan. However, the mechanisms behind this phenomenon are not well understood. Here, using genetic loss-of-function models for fibroblast growth factor 21 (Fgf21) and its obligate co-receptor β-Klotho (Klb), we demonstrate that FGF21-KLB signalling in adipocytes is indispensable for the anti-senescence effects of PR. Specifically, adipocyte FGF21 signalling preserves mitochondrial integrity, maintains an anti-inflammatory milieu and sustains nicotinamide adenine dinucleotide (NAD

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Research summary

Adipocyte FGF21-KLB signalling is indispensable for the anti-senescence effects of protein restriction by preserving mitochondrial integrity and maintaining an anti-inflammatory milieu. This paper identifies a specific molecular mechanism (FGF21 signaling in adipocytes) that mediates the lifespan-extending benefits of dietary protein restriction, providing a crucial mechanistic link between nutritional intervention and cellular aging processes.

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