Abstract
The aim of this study was to identify peptides in chickpea protein hydrolysate (CPH) capable of ameliorating the metabolic consequences of a high-fat diet (HFD) using a model of metabolic dysfunction. C57BL/6J male mice were randomly divided into three groups (n = 13/group) and fed for 12 weeks a HFD + 0 mg CPH/kg body weight (BW) (0 CPH), HFD + 400 mg CPH/kg BW (400 CPH), or HFD + 800 mg CPH/kg BW (800 CPH). At the end, BW reduction in the 800 CPH group was 24.8 % compared to the control group (0 CPH) (p < 0.01). The 0 CPH group had the highest NAFLD score, and the 800 CPH group had the lowest. In liver, 400 CPH downregulated genes (fold change [FC] >1 or <−1) related to long-chain fatty acid uptake (Slc27a1), adipokine signaling (Tnfrsf1b) and insulin signaling (Pik3r1, Ikbkb, and Map2k1). CPH prevents NAFLD development by regulating inflammation and preventing steatosis via lipogenesis.
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