The secreted peptide BATSP1 promotes thermogenesis in adipocytes.
Xianwei CuiHong ZhongYangyang WuZhuo ZhangXiaoxiao ZhangLu LiJin HeChen ChenZhenggang WuXianwei CuiPublished in: Cellular and molecular life sciences : CMLS (2023)
Although brown adipose tissue (BAT) has historically been viewed as a major site for energy dissipation through thermogenesis, its endocrine function has been increasingly recognized. However, the circulating factors in BAT that play a key role in controlling systemic energy homeostasis remain largely unexplored. Here, we performed a peptidomic analysis to profile the extracellular peptides released from human brown adipocytes upon exposure to thermogenic stimuli. Specifically, we identified a secreted peptide that modulates adipocyte thermogenesis in a cell-autonomous manner, and we named it BATSP1. BATSP1 promoted BAT thermogenesis and induced browning of white adipose tissue in vivo, leading to increased energy expenditure under cold stress. BATSP1 treatment in mice prevented high-fat diet-induced obesity and improved glucose tolerance and insulin resistance. Mechanistically, BATSP1 facilitated the nucleocytoplasmic shuttling of forkhead transcription factor 1 (FOXO1) and released its transcriptional inhibition of uncoupling protein 1 (UCP1). Overall, we provide a comprehensive analysis of the human brown adipocyte extracellular peptidome following acute forskolin (FSK) stimulation and identify BATSP1 as a novel regulator of thermogenesis that may offer a potential approach for obesity treatment.
Keyphrases
- replacement therapy
- adipose tissue
- insulin resistance
- high fat diet induced
- transcription factor
- high fat diet
- polycystic ovary syndrome
- endothelial cells
- high glucose
- drug induced
- metabolic syndrome
- gene expression
- glycemic control
- signaling pathway
- type diabetes
- oxidative stress
- cell therapy
- risk assessment
- weight loss
- hepatitis b virus
- single cell
- body mass index
- bone marrow
- intensive care unit
- combination therapy
- human health
- heat stress
- fatty acid
- physical activity
- extracorporeal membrane oxygenation
- pluripotent stem cells
- mesenchymal stem cells
- heat shock
- climate change
- aortic dissection