Abstract
Obesity and related metabolic syndromes are among the top public health issues worldwide. The current strategy is mainly based on controlling food intake, unable to achieve the optimal treatment effect. How to augment energy expenditure becomes a new focus. White adipose tissue (WAT) is a classic energy storage depot, whereas brown adipose tissue (BAT) dissipates energy through thermogenesis. Browning of WAT facilitates the transformation from WAT into beige adipose tissue acquiring modest thermogenic activity. Enhancement of thermogenic function of both BAT and beige adipose tissue highlights a novel perspective to dissipate excess stored energy and reduce lipid deposition. In this review, we systematically summarize the current regulatory mechanisms of thermogenesis revealed in BAT and beige adipose tissue, including the thermogenic function of mitochondria, the crosstalk between macrophages and adipocytes, endoplasmic reticulum stress as well as proteasome activity. Additionally, we discuss the underlying signaling network to regulate relevant gene expression involved in these four aspects so as to provide a better understanding for therapeutic strategy design to treat obesity and related metabolic diseases.
Highlights
Obesity and related metabolic syndromes have been one of the most concerned public health problems worldwide [1]
According to the structure and function of adipocytes, adipose tissue is classified into white adipose tissue (WAT) and brown adipose tissue (BAT)
LPS activated TLR4 signaling activated reduces thermogenesis related with reduced body temperature and brown-specific genes such as uncoupled protein 1 (UCP1) and PRDM16, as well as promote obesity related with ER stress and increased CCAAT enhancer binding protein homologous protein (CHOP) expression [61]
Summary
Obesity and related metabolic syndromes have been one of the most concerned public health problems worldwide [1]. We explore and summarize the mechanisms mainly related to the thermogenic function of mitochondria, the infiltrated macrophages, ER (endoplasmic reticulum) stress and proteasomal activity in brown and beige adipocytes. The expression of UCP1 in beige adipose tissue is lower than BAT [15], and chronic treatment with β3-AR agonist increases respiration of epididymal WAT in UCP1−/− mice [16].
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