Overview of growth differentiation factor 15 (GDF15) in metabolic diseases

被引:7
|
作者
Li, Jian [1 ]
Hu, Xiangjun [2 ]
Xie, Zichuan [2 ]
Li, Jiajin [2 ]
Huang, Chen [3 ,4 ,5 ]
Huang, Yan [3 ]
机构
[1] Sichuan Univ, Inst Kidney Dis, Dept Nephrol, West China Hosp, Chengdu, Peoples R China
[2] Sichuan Univ, West China Sch Med, Chengdu, Peoples R China
[3] Sichuan Univ, West China Hosp, Hlth Management Ctr, Gen Practice Med Ctr, Chengdu, Peoples R China
[4] Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy, Chengdu 610041, Sichuan, Peoples R China
[5] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Sichuan, Peoples R China
关键词
GDF15; GFRAL; Metabolism; Appetite regulation; Obesity; Anorexia; MACROPHAGE INHIBITORY CYTOKINE-1; BETA SUPERFAMILY MEMBER; PROMOTES WEIGHT-LOSS; HEPATOCELLULAR-CARCINOMA; INSULIN-RESISTANCE; BODY-COMPOSITION; TRANSGENIC MICE; FOOD-INTAKE; OBESITY; CANCER;
D O I
10.1016/j.biopha.2024.116809
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
GDF15 is a stress response cytokine and a distant member of the transforming growth factor beta (TGF beta) superfamily, its levels increase in response to cell stress and certain diseases in the serum. To exert its effects, GDF15 binds to glial-derived neurotrophic factor (GDNF) receptor alpha-like (GFRAL), which was firstly identified in 2017 and highly expressed in the brain stem. Many studies have demonstrated that elevated serum GDF15 is associated with anorexia and weight loss. Herein, we focus on the biology of GDF15, specifically how this circulating protein regulates appetite and metabolism in influencing energy homeostasis through its actions on hindbrain neurons to shed light on its impact on diseases such as obesity and anorexia/cachexia syndromes. It works as an endocrine factor and transmits metabolic signals leading to weight reduction effects by directly reducing appetite and indirectly affecting food intake through complex mechanisms, which could be a promising target for the treatment of energy-intake disorders.
引用
收藏
页数:11
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