Overview of growth differentiation factor 15 in metabolic syndrome

Abstract

Growth and differentiation factor 15 (GDF15) is a member of the transforming growth factor‐β (TGF‐β) superfamily. GDF15 has been linked with several metabolic syndrome pathologies such as obesity and cardiovascular diseases. GDF15 is considered to be a metabolic regulator, although its precise mechanisms of action remain to be determined. Glial cell‐derived neurotrophic factor family receptor alpha‐like (GRAL), located in the hindbrain, has been identified as the receptor for GDF15 and signals through the coreceptor receptor tyrosine kinase (RET). Administration of GDF15 analogues in preclinical studies using various animal models has consistently been shown to induce weight loss through a reduction in food intake. GDF15, therefore, represents an attractive target to combat the current global obesity epidemic. In this article, we review current knowledge on GDF15 and its involvement in metabolic syndrome.

A method of quantitative chemiluminescence immunoassay for the concentration of Growth differentiation factor-15

“…3 ). These data are consistent with previous findings that GDF-15 levels raise significantly in cardiovascular disease compared to healthy controls [ 1 , [8] , [9] , [10] ]. Therefore, we conclude that our chemiluminescence immunoassay is a reliable method for analyzing serum GDF-15 concentration in clinical and in vivo studies.…”

Research Progress on the Role and Mechanism of GDF15 in Body Weight Regulation

“…Johnen et al [32] observed that after 6 months of a HFD, ApoE(−/−) mice overexpressing GDF15 had smaller atherosclerotic lesions. The protective effect of GDF15 on the cardiovascular system has also been confirmed by many studies [33,34]. These findings suggest that GDF15 may help counteract some of the detrimental effects of obesity on the cardiovascular system.…”

Sarcopenic obesity: epidemiology, pathophysiology, cardiovascular disease, mortality, and management

“…Growth differentiation factor 15 (GDF15) has been implicated in aging, inflammation, mitochondrial dysfunction, cachexia, and sarcopenia ( 34 , 35 ). It is likely that these changes are also altered in patients with sarcopenic obesity; however, this needs to be confirmed.…”