A high-fat diet induced obesity, leading to brown adipose tissue inflammation, reduced insulin signaling, and impaired glucose uptake in mice compared to a normal chow diet.
Does a high-fat diet cause insulin resistance and inflammation in brown adipose tissue in mice?
Diet-induced obesity leads to inflammation and insulin resistance in brown adipose tissue, impairing its thermogenic and metabolic function.
OBJECTIVE: Diet-induced obesity (DIO) causes several pathophysiological changes in adipose tissue. Increased inflammation reduces white adipose tissue (WAT) insulin sensitivity and contributes to the development of diabetes. However, little is known about how DIO alters the function of brown adipose tissue (BAT), an organ that consumes calories by β3-adrenergic receptor (AR)-mediated thermogenesis and helps regulate energy balance. METHODS: To test the effects of DIO on BAT, we fed 6-week-old C57BL/6 mice either a normal chow diet (NCD) or a high-fat diet (HFD). After 16 additional weeks, we measured body fat, WAT, and BAT mRNA expression, glucose tolerance, and rates of glucose uptake in response to insulin and the β3-AR agonist mirabegron. RESULTS: Compared with NCD, HFD increased body fat and impaired glucose tolerance. Both WAT and BAT had higher mRNA levels of markers of inflammation, including TNFα and F4/80. Insulin signaling in BAT and WAT was reduced, with decreased Akt phosphorylation. Diet-normalized BAT glucose uptake rates were lower in response to mirabegron. CONCLUSIONS: These results support a model in which DIO leads to BAT inflammation and insulin resistance, leading to a broader impairment of BAT function.
Roberts‐Toler et al. (Mon,) conducted a other in Diet-induced obesity. High-fat diet (HFD) vs. Normal chow diet (NCD) was evaluated on Body fat, WAT and BAT mRNA expression, glucose tolerance, and glucose uptake. A high-fat diet induced obesity, leading to brown adipose tissue inflammation, reduced insulin signaling, and impaired glucose uptake in mice compared to a normal chow diet.
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