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

Journal
Journal of Food and Drug Analysis
Journal Volume
29
Journal Issue
2
Pages
375-388
Date Issued
2021
Author(s)
Wu, Yi-Hsieng Samuel
Lin, Yi-Ling
WEN-YUAN YANG  
SHENG-YAO WANG  orcid-logo
YI-CHEN CHEN  
DOI
10.38212/2224-6614.3351
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85110287231&doi=10.38212%2f2224-6614.3351&partnerID=40&md5=db1b2a60d5f3cba469d131d9447f19db
https://scholars.lib.ntu.edu.tw/handle/123456789/605778
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 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 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. ? 2021, Taiwan Food and Drug Administration. All rights reserved.
Subjects
Adipose tissue
Chicken-liver hydrolysates
Insulin resistance
Non-alcoholic fatty liver disease
Skeletal muscle
alanine aminotransferase
albumin
alkaline phosphatase
aspartate aminotransferase
catalase
fatty acid
glucose
glutathione
glutathione peroxidase
insulin
interleukin 1beta
ketone body
liver protective agent
oleic acid
pepsin A
protein hydrolysate
superoxide dismutase
thiobarbituric acid reactive substance
triacylglycerol
tumor necrosis factor
alanine aminotransferase blood level
albumin blood level
alkaline phosphatase blood level
animal cell
animal experiment
animal model
animal tissue
Article
aspartate aminotransferase blood level
body weight gain
cell degeneration
chicken
cholesterol blood level
controlled study
eating habit
fatty acid blood level
fatty liver
FL83B cell line
glucose blood level
in vitro study
in vivo study
insulin resistance
lipid diet
lipid storage
liver protection
liver tissue
male
mouse
nonhuman
steatosis
stimulation
triacylglycerol blood level
trolox equivalent antioxidant capacity
upregulation
SDGs

[SDGs]SDG3

Type
journal article

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