Konjac glucomannan attenuate high-fat diet-fed obesity through enhancing β-adrenergic-mediated thermogenesis in inguinal white adipose tissue in mice.

Abstract

Konjac glucomannan (KGM) has been reported to prevent high-fat diet-induced obesity, and we study investigated whether dietary supplementation with KGM can prevent obesity by increasing energy expenditure in inguinal white adipose tissue (iWAT) of high-fat diet (HF) -fed mice. Weaned mice fed the control diet (Con), HF, or HF plus KGM (8%, w/w, HFK) were divided into three groups. The results showed that 10-week supplementation with KGM significantly reduced partial adipose tissue weight and body weight, and improved glucose tolerance. Compared to the HF group, plasma lipid concentrations in the HFK group were greatly decreased to the control level. Moreover, transcriptomic research has shown that genes that are mainly associated with energy and lipid metabolism are significantly altered in iWAT. Mechanistically, KGM stimulated thermogenesis by promoting the expression of uncoupling protein-1 (UCP1) and the β3-adrenergic receptor (ADR3β). Taken together, our results suggest that dietary supplementation with konjac glucomannan can effectively alleviate obesity induced by a high-fat diet by activating ADR3β-mediated iWAT thermogenesis. Dietary supplementation with KGM can effectively alleviate high fat diet- induced obesity mice by via activating ADR3β-mediated thermogenesis of iWAT.