Fuzhuan brick tea extract prevents diet-induced obesity via stimulation of fat browning in mice.

Fuzhuan brick tea is a post-fermented tea that is intentionally fermented by the fungus Eurotium cristatum. Previous studies have reported the anti-obesity effect of Fuzhuan brick tea extracts (FBT), but the underlying mechanism remains unclear. The present study investigated whether FBT exerts anti-obesity effects through energy expenditure and browning of white adipose tissue. Mice were administered 100 mg or 200 mg FBT/kg body weight along with a high-fat diet (HFD) for 12 weeks; the FBT group had a significantly reduced body weight and adipose tissue mass compared to mice fed an HFD alone. FBT also improved serum biochemical parameters and hepatic steatosis concomitant with obesity. Furthermore, FBT enhanced energy expenditure and promoted browning of subcutaneous adipose tissue by upregulating the expression of brown adipocyte-specific genes, including uncoupling protein 1. Based on these results, we suggest that FBT induces energy expenditure by promoting the browning of subcutaneous adipose tissue, which prevents weight gain.

Coumarin attenuates hepatic steatosis by down-regulating lipogenic gene expression in mice fed a high-fat diet.

Coumarin is a natural compound abundant in plant-based foods such as citrus fruits, tomatoes, vegetables and green tea. Although coumarin has been reported to exhibit anti-coagulant, anti-inflammation and cholesterol-lowering properties, the effect of coumarin on hepatic lipid metabolism remains unclear. In the present study, we evaluated the ability of coumarin to protect against hepatic steatosis associated with a high-fat diet (HFD) and investigated potential mechanisms underlying this effect. C57BL/6J mice were fed a normal diet, HFD and HFD containing 0·05 % courmarin for 8 weeks. The present results showed that coumarin reduced weight gain and abdominal fat mass in mice fed the HFD for 8 weeks (P< 0·05). Coumarin also significantly reduced the HFD-induced elevation in total cholesterol, apoB, leptin and insulin (P< 0·05). In the liver of HFD-fed mice, coumarin significantly reduced total lipids, TAG and cholesterol (38, 22 and 9 % reductions, respectively; P< 0·05), as well as lipid droplet number and size. Additionally, thiobarbituric acid-reactive substance levels, as an indicator of hepatic steatosis, were attenuated by coumarin (P< 0·05). Finally, coumarin suppressed the HFD-induced up-regulation in fatty acid synthase (FAS) activity, and the expression of sterol regulatory element-binding protein-1, FAS, acetyl-CoA carboxylase 1, PPARγ and CCAAT/enhancer-binding protein-α in the liver. Taken together, these results demonstrate that coumarin could prevent HFD-induced hepatic steatosis by regulating lipogenic gene expression, suggesting potential targets for preventing hepatic steatosis.