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. 2022 Jan 25;12:788549. doi: 10.3389/fendo.2021.788549

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Copyright © 2022 Wang, Feng, Wang, Dong, Wang, Zhong, Li, Fu, Xiao, Speakman, Li and Gao

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A proposed mechanistic model for interaction between ANGPTL8 and leptin on LVH through triglyceride. The hepatokine ANGPTL8 might facilitate angiopoietin-like protein 3 (ANGPTL3) to inhibit lipoprotein lipase (LPL) activity for conversion of triglyceride (TG) into fatty acids (FAs) in myocardium, resulting in increased circulating TG and decreased FAs uptake into cardiomyocytes, and coordinating the trafficking of TG to white adipose tissue for storage, and ultimately, inducing higher leptin secretion. Meanwhile, high leptin levels might stimulate β-oxidation of FAs and inhibit de novo lipogenesis in cardiomyocytes to further prevent myocardial TG accumulation and lipid cardiomyopathy, leading to a favorable LVMI. Thereby, the adipokine leptin and the hepatokine ANGPTL8 cooperate together to decrease cardiac TG involved in mechanism of protective effect on cardiac remodeling.