Search

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., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

As obesity promotes ectopic fat accumulation in skeletal muscle, resulting in impaired skeletal muscle and mitochondria function, it is associated with skeletal muscle loss and dysfunction. This study investigated whether Chrysanthemi zawadskii var. latilobum (CZH) protected mice against obesity-induced skeletal muscle atrophy and the underlying molecular mechanisms. High-fat diet (HFD)-induced obese mice were orally administered either distilled water, low-dose CZH (125 mg/kg), or high-dose CZH (250 mg/kg) for 8 w. CZH reduced obesity-induced increases in inflammatory cytokines levels and skeletal muscle atrophy, which is induced by expression of atrophic genes such as muscle RING-finger protein 1 and muscle atrophy F-box. CZH also improved muscle function according to treadmill running results and increased the muscle fiber size in skeletal muscle. Furthermore, CZH upregulated mRNA and protein levels of protein arginine methyltransferases (PRMT)1 and PRMT7, which subsequently attenuated mitochondrial dysfunction in the skeletal muscle of obese mice. We also observed that CZH significantly decreased PRMT6 mRNA and protein expression, which resulted in decreased muscle atrophy. These results suggest that CZH ameliorated obesity-induced skeletal muscle atrophy in mice via regulation of PRMTs in skeletal muscle.

The DNA damage response is essential for preserving genome integrity and eliminating damaged cells. Although cellular metabolism plays a central role in cell fate decision between proliferation, survival, or death, the metabolic response to DNA damage remains largely obscure. Here, this work shows that DNA damage induces fatty acid oxidation (FAO), which is required for DNA damage‐induced cell death. Mechanistically, FAO induction increases cellular acetyl‐CoA levels and promotes N‐alpha‐acetylation of caspase‐2, leading to cell death. Whereas chemotherapy increases FAO related genes through peroxisome proliferator‐activated receptor α (PPARα), accelerated hypoxia‐inducible factor‐1α stabilization by tumor cells in obese mice impedes the upregulation of FAO, which contributes to its chemoresistance. Finally, this work finds that improving FAO by PPARα activation ameliorates obesity‐driven chemoresistance and enhances the outcomes of chemotherapy in obese mice. These findings reveal the shift toward FAO induction is an important metabolic response to DNA damage and may provide effective therapeutic strategies for cancer patients with obesity. [ABSTRACT FROM AUTHOR]