ZHANG Xin
Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, ChinaYANG Ying
Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, ChinaAN Xiaoyu
1.Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, China. 2. Graduate School, Inner Mongolia Medical University, Hohhot 010110GU Yanqi
Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, ChinaZHANG Yin
Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, ChinaMA Yan
Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, ChinaSUN Liting
Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, ChinaLIN Fang
Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, ChinaWU Qiangqiang
1.Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, China. 2. Graduate School, Inner Mongolia Medical University, Hohhot 010110WANG Yana
1.Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, China. 2. Graduate School, Inner Mongolia Medical University, Hohhot 010110YANG Huidi
Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, China1.Basic Medical School, Inner Mongolia Medical University, Hohhot 010110, China. 2. Graduate School, Inner Mongolia Medical University, Hohhot 010110
Objective To explore the mechanism by which docosahexaenoic acid ( DHA) inhibits the accumulation of adipose tissue lipid in high-fat diet ( HFD)-induced body weight gain in C57BL/ 6 mice. Methods Animals were fed a control diet (C57BL/ 6 C group), a 45% HFD (C57BL/ 6 H group) or 45% HFD with 0. 2 g DHA (FAD3C) or 0. 4 g DHA (FAD3H) per g of food for 20 weeks. Resting metabolic rate was measured at 19 weeks. Visceral adipose and brown adipose tissue were collected for RNA extraction. Lipogenesis-related and fat browning-related gene expression was detected by quantitative PCR. Results A HFD significantly increased (P < 0. 05) body weight, body fat, and serum leptin and triglyceride ( TG) levels in the C57BL/ 6 H group compared with the C57BL/ 6 C group. DHA significantly decreased (P < 0. 05) body weight, fat mass, and levels of serum leptin and TG in the FAD3C and FAD3H groups compared with the C57BL/ 6 H group. In visceral adipose tissue, DHA significantly downregulated the expression of lipogenesis-related genes, including the CCAAT/ enhancer-binding protein, peroxisome proliferator-activated receptor-γ, and sterol regulatory element-binding protein-1C in FAD3H groups compared with the C57BL/ 6 C group (P < 0. 05). In visceral adipose and brown adipose tissue, DHA supplementation significantly increased (P < 0. 05) the expression of fat browning-related genes, including uncoupling protein 1, and peroxisome proliferator-activated receptor coactivator-1a in FAD3H groups compared with the C57BL/ 6 H group. Conclusions DHA may be used to combat obesity by regulating the resting metabolic rate, levels of leptin, fat and TG, and the expression of browning-related and lipogenesis-related genes.
