Βeta-glucan suppresses high-fat-diet-induced obesity by attenuating dyslipidemia and modulating obesogenic marker expressions in rats

The current study was designed to evaluate the therapeutic potential of beta-glucan (BG), which is a key bioactive compound predominantly present in mushrooms and cereals against high-fat-diet (HFD)-induced obesity, and to understand its mechanism of action. Obesity was induced in rats by supplementing the diet with HFD and BG (40 mg/kg body weight) for a period of 6 weeks. At the end of the experimental period, the body weight, as well as hyperglycemic, dyslipidemia, and obesogenic marker expressions, was assessed in the control group and in the experimental obese rats. Administration of BG to obese rats significantly reduced body weight gain and attenuated hyperglycemia, which was confirmed by the decreased blood glucose and insulin resistance. At the same time, BG mitigated dyslipidemia by altering expressions of peroxisome proliferator-activated receptor-gamma (PPAR-gamma), sterol regulatory element-binding protein 1 (SREBP-1c), fatty acid synthase (FAS), 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, and fatty acid-binding protein-4 (Fab-4) in HFD-induced obese rats. In conclusion, this study revealed that BG is a potential candidate to ameliorate HFD-induced obesity by modulating obesogenic marker expressions, especially by regulating the master regulator PPAR-gamma.

Automated summary

The study examined the therapeutic potential of beta-glucan (BG) found in mushrooms and cereals against high-fat-diet-induced obesity. Rats were fed a high-fat diet with BG supplementation for 6 weeks, resulting in reduced body weight gain and improved hyperglycemia. BG also mitigated dyslipidemia by regulating the expressions of key markers associated with obesity. The study concluded that BG is a potential candidate for treating high-fat-diet-induced obesity by modulating obesogenic marker expressions, specifically the master regulator PPAR-gamma.