4.7 Article

Omega-3 Polyunsaturated Fatty Acids Protect against High-Fat Diet-Induced Morphological and Functional Impairments of Brown Fat in Transgenic Fat-1 Mice

期刊

出版社

MDPI
DOI: 10.3390/ijms231911903

关键词

obesity; omega-3 fatty acids; fat-1 transgenic mice; brown adipose tissue; energy homeostasis; thermogenesis; lipopolysaccharide; inflammation

资金

  1. Sansun Life Sciences (Hong Kong)
  2. Fortune Education Foundation (New York)

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This study utilized a transgenic fat-1 mouse model to investigate the regulation of brown adipose tissue (BAT) morphology and function by n-3 polyunsaturated fatty acids (n-3 PUFAs). The findings showed that elevated tissue levels of n-3 PUFAs can alleviate high-fat diet-induced obesity by enhancing thermogenesis and reducing inflammation in BAT.
The role of omega-3 polyunsaturated fatty acids (n-3 PUFAs) in the regulation of energy homeostasis remains poorly understood. In this study, we used a transgenic fat-1 mouse model, which can produce n-3 PUFAs endogenously, to investigate how n-3 PUFAs regulate the morphology and function of brown adipose tissue (BAT). We found that high-fat diet (HFD) induced a remarkable morphological change in BAT, characterized by whitening due to large lipid droplet accumulation within BAT cells, associated with obesity in wild-type (WT) mice, whereas the changes in body fat mass and BAT morphology were significantly alleviated in fat-1 mice. The expression of thermogenic markers and lypolytic enzymes was significantly higher in fat-1 mice than that in WT mice fed with HFD. In addition, fat-1 mice had significantly lower levels of inflammatory markers in BAT and lipopolysaccharide (LPS) in plasma compared with WT mice. Furthermore, fat-1 mice were resistant to LPS-induced suppression of UCP1 and PGC-1 expression and lipid deposits in BAT. Our data has demonstrated that high-fat diet-induced obesity is associated with impairments of BAT morphology (whitening) and function, which can be ameliorated by elevated tissue status of n-3 PUFAs, possibly through suppressing the effects of LPS on inflammation and thermogenesis.

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