Knockout of RAP1B in Adipose Tissue Decreases Fat Accumulation in Obese Mice under Cold Conditions
FU Yinxu1, ZHU Hui1, WANG Xinbo1, HU Pingyi2, FANG Yu2, ZHOU Huaibin1, LÜ Jianxin1,2*
This study aims to explore the role of RAP1B in regulating metabolic functions in adipose tissue and its implications in obesity. Using adipose tissue-specific Rap1b knockout mice subjected to HFD (highfat diet) feeding and cold exposure, along with RAP1B knockdown 3T3-L1 cell models, the impact of RAP1B on mitochondrial function was systematically analyzed in white adipose tissue. By comparing Rap1b knockout mice with control mice, body weight, fat content, lipid metabolism indicators, and thermoregulation ability were assessed in adipose tissue. Results revealed that RAP1B-deficient mice exhibited significantly elevated nocturnal body temperature and reduced fat content under HFD conditions. In 3T3-L1 cells, RAP1B knockdown did not affect adipocyte differentiation or lipid accumulation but significantly enhanced mitochondrial respiratory function and ATP production. Further investigations showed that RAP1B deficiency markedly increased mitochondrial complex content in both mouse adipose tissue and 3T3-L1 cells. Proteomic analysis of adipose tissue indicated enrichment in oxidative phosphorylation and thermogenic pathways. These findings suggest that RAP1B may improve adipose tissue metabolic capacity by enhancing mitochondrial function, thereby influencing thermoregulation and lipid storage. This study highlights the critical role of RAP1B in regulating mitochondrial function in adipose tissue and proposes that RAP1B may impact the development of obesity by modulating mitochondrial activity and lipid metabolism.
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