Lactobacillus plantarum dy-1 fermented barley extraction activates white adipocyte browning in high-fat diet-induced obese rats.

Abstract

High-fat diet (HFD)-induced obesity is caused by the imbalance between energy intake and expenditure. Here, we studied the inhibitory effects of aqueous extracts of fermented barley with Lactobacillus plantarum dy-1 (LFBE) and beta-glucan (BGL) on the obesity induced by HFD. Both LFBE and BGL significantly decreased body weight, suppressed visceral lipid accumulation, improved blood lipid profile, and glucose tolerance in HFD rats. BGL showed no thermogenic capacity, while LFBE enhanced the expression of Uncoupling Protein 1 (UCP1), and brown-specific mRNA (PRDM16, PGC1-α, and CIDEA) levels in brown adipose tissue (BAT) and white adipose tissues (WAT) of HFD rats. In addition, LFBE increased the expression of key genes involved in mitochondria biosynthesis and the mitochondrial respiration function. Further, we demonstrated that proteins extracted from LFBE (LFBE-P) were responsible for triggering brown markers to some extent. In conclusion, LFBE alleviates HFD-induced obesity by activating thermogenic fat bioenergetics and mitochondria biosynthesis. PRACTICAL APPLICATIONS: Barley is one of the most productive crops with pretty low utilization. Our group committed to exploring the application and nutritional value of barley. This work aimed to explore improvements in nutritional function of barley after fermentation by Lactobacillus plantarum dy-1. Our study found that oral administration of LFBE help turning white adipose tissue into a thermogenesis state and activate heat generation function of brown adipose tissue. Its characteristics mentioned above significantly inhibited the body weight and blood lipid of high-fat diet rats. Further, we evidenced that LFBE-P were responsible for triggering brown markers in 3T3-L1 cells. We believe our research plays a great part to relieving high-fat diet-induced obesity and type 2 diabetes with functional diet supplementation.