Nature metabolism · 2022
Body weight regulation via MT1-MMP-mediated cleavage of GFRAL.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Chow Chi Fung Willis, Guo Xuanming, Asthana Pallavi, Zhang Shuo, Wong Sheung Kin Ken, Fallah Samane, Che Sijia, Gurung Susma, Wang Zening, Lee Ki Baek, Ge Xin, Yuan Shiyang, Xu Haoyu, Ip Jacque Pak Kan, Jiang Zhixin, Zhai Lixiang, Wu Jiayan, Zhang Yijing, Mahato Arun Kumar, Saarma Mart, Lin Cheng Yuan, Kwan Hiu Yee, Huang Tao, Lyu Aiping, Zhou Zhongjun, Bian Zhao-Xiang, Wong Hoi Leong Xavier
Аннотация
GDNF-family receptor a-like (GFRAL) has been identified as the cognate receptor of growth/differentiation factor 15 (GDF15/MIC-1), considered a key signaling axis in energy homeostasis and body weight regulation. Currently, little is known about the physiological regulation of the GDF15-GFRAL signaling pathway. Here we show that membrane-bound matrix metalloproteinase 14 (MT1-MMP/MMP14) is an endogenous negative regulator of GFRAL in the context of obesity. Overnutrition-induced obesity increased MT1-MMP activation, which proteolytically inactivated GFRAL to suppress GDF15-GFRAL signaling, thus modulating the anorectic effects of the GDF15-GFRAL axis in vivo. Genetic ablation of MT1-MMP specifically in GFRAL+ neurons restored GFRAL expression, resulting in reduced weight gain, along with decreased food intake in obese mice. Conversely, depletion of GFRAL abolished the anti-obesity effects of MT1-MMP inhibition. MT1-MMP inhibition also potentiated GDF15 activity specifically in obese phenotypes. Our findings identify a negative regulator of GFRAL for the control of non-homeostatic body weight regulation, provide mechanistic insights into the regulation of GDF15 sensitivity, highlight negative regulators of the GDF15-GFRAL pathway as a therapeutic avenue against obesity and identify MT1-MMP as a promising target.