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; Yi-Ling Lin; Wen-Yuan Yang; Sheng-Yao Wang; Yi-Chen Chen

doi:10.38212/2224-6614.3351

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

J Food Drug Anal. 2021 Jun 15;29(2):375-388. doi: 10.38212/2224-6614.3351.

Authors

Yi-Hsieng Samuel Wu¹, Yi-Ling Lin¹, Wen-Yuan Yang², Sheng-Yao Wang¹, Yi-Chen Chen¹

Affiliations

¹ Department of Animal Science and Technology, National Taiwan University, Taipei, 106, Taiwan.
² Department of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, Taipei, 106, Taiwan.

Abstract

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 μM 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 in HFD-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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Body Weight
Chickens
Fatty Liver* / drug therapy
Feeding Behavior
Glucose
Insulin
Insulin Resistance*
Mice
Pepsin A

Substances

Insulin
Pepsin A
Glucose

Grants and funding

We acknowledge funding for this research from the Ministry of Science and Technology, Taiwan (Project: MOST 106-2313-B-002-040-MY3 and MOST 109-2313-B-002-007-MY3) and Council of Agriculture, Executive Yuan, Taiwan (Project: 107AS-15.4.1- ST-a5, 108AS-14.1.1-ST-a2, and 109AS-12.1.1-ST-a1).