Pepsin-digested chicken-liver hydrolysate attenuates hepatosteatosis by relieving hepatic and peripheral insulin resistance in long-term high-fat dietary habit

Yi-Hsieng Samuel Wu ^a, Yi-Ling Lin ^a, Wen-Yuan Yang ^b, Sheng-Yao Wang ^a, Yi-Chen Chen ^a,*

a Department of Animal Science and Technology, National Taiwan University, Taipei, 106, Taiwan

b Department of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, Taipei, 106, Taiwan

This study aims to clarify the effects of chicken liver hydrolysates (CLHs) on long-term high-fat diet (HFD)-induced insulin resistance (IR) and hepatosteatosis in mice. In vitro, the 400 mM oleic acid (OA)-added medium successfully stimulated the cellular steatosis on FL83B cells, and the cellular steatosis was attenuated ( p < 0.05) by supplementing with CLHs (4 mg/L). In vivo, the effects of CLHs on IR and hepatosteatosis development were tested in 20-week HFD-fed mice. HFD-induced increases in final body weight, but body weight gains of mice were decreased ( p < 0.05) by supplementing CLHs. Elevated ( p < 0.05) serum aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), free fatty acids (FFAs), triglyceride (TG), total cholesterol (TC), and fasted glucose values inHFD-fed mice decreased ( p < 0.05) by supplementing CLHs. Both results of hepatic steatosis and fibrotic scores also indicated the retardation ( p < 0.05) of the hepatosteatosis in cotreated groups. Moreover, the CLH supplementation sustained ( p < 0.05) hepatic and peripheral insulin signal sensitivity in HFD-fed mice. CLH supplementation could ameliorate hepatic lipid deposition, hepatic/peripheral IR in a long-term high-fat dietary habit, and also improve the universal glucose homeostasis by upregulating hepatic and peripheral insulin sensitivities.

Keywords: Adipose tissue, Chicken-liver hydrolysates, Insulin resistance, Non-alcoholic fatty liver disease, Skeletal muscle

https://doi.org/10.38212/2224-6614.3351

(https://www.jfda-online.com/journal/vol29/iss2/13)