Regulation of adipose tissue development and energy metabolism by VEGFB isoforms

Author:

Chen Yang12ORCID,Li Xin1,Zhang Jing2,Zhang Mingjiao2,Adlat Salah2,Lu Xiaodan2,Li Dan2,Jin Honghong2,Wang Chenhao2,Mar Oo Zin2,Hayel Farooq2,Chen Quangang1,Han Xufeng1,Chen Renjin1ORCID,Feng Xuechao2,Zhang Luqing2,Zheng Yaowu2ORCID

Affiliation:

1. School of Life Science, Xuzhou Medical University, Xuzhou, Jiangsu, China

2. Transgenic Research Center, Northeast Normal University, Changchun, Jilin, China

Abstract

Obesity is caused by imbalanced energy intake and expenditure. Excessive energy intake and storage in adipose tissues are associated with many diseases. Several studies have demonstrated that vascular growth endothelial factor B (VEGFB) deficiency induces obese phenotypes. However, the roles of VEGFB isoforms VEGFB167 and VEGFB186 in adipose tissue development and function are still not clear. In this study, genetic mouse models of adipose-specific VEGFB167 and VEGFB186 overexpression (aP2-Vegfb167 tg/+and aP2-Vegfb186tg/+) were generated and their biologic roles were investigated. On regular chow, adipose-specific VEGFB186 is negatively associated with white adipose tissues (WATs) and positively regulates brown adipose tissues (BATs). VEGFB186 upregulates energy metabolism and metabolism-associated genes. In contrast, VEGFB167 has a nominal role in adipose development and function. On high-fat diet, VEGFB186 expression can reverse the phenotypes of VEGFB deletion. VEGFB186 overexpression upregulates BAT-associated genes and downregulates WAT-associated genes. VEGFB186 and VEGFB167 have very distinct roles in the regulation of adipose development and energy metabolism. As a key regulator of adipose tissue development and energy metabolism, VEGFB186 may be a target for obesity prevention and treatment.

Publisher

Bioscientifica

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism

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