Wu, Yi-Hsieng SamuelYi-Hsieng SamuelWuLin, Yi-LingYi-LingLinWEN-YUAN YANGSHENG-YAO WANGYI-CHEN CHEN2022-04-252022-04-25202110219498https://www.scopus.com/inward/record.uri?eid=2-s2.0-85110287231&doi=10.38212%2f2224-6614.3351&partnerID=40&md5=db1b2a60d5f3cba469d131d9447f19dbhttps://scholars.lib.ntu.edu.tw/handle/123456789/605778This 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.Adipose tissueChicken-liver hydrolysatesInsulin resistanceNon-alcoholic fatty liver diseaseSkeletal musclealanine aminotransferasealbuminalkaline phosphataseaspartate aminotransferasecatalasefatty acidglucoseglutathioneglutathione peroxidaseinsulininterleukin 1betaketone bodyliver protective agentoleic acidpepsin Aprotein hydrolysatesuperoxide dismutasethiobarbituric acid reactive substancetriacylglyceroltumor necrosis factoralanine aminotransferase blood levelalbumin blood levelalkaline phosphatase blood levelanimal cellanimal experimentanimal modelanimal tissueArticleaspartate aminotransferase blood levelbody weight gaincell degenerationchickencholesterol blood levelcontrolled studyeating habitfatty acid blood levelfatty liverFL83B cell lineglucose blood levelin vitro studyin vivo studyinsulin resistancelipid dietlipid storageliver protectionliver tissuemalemousenonhumansteatosisstimulationtriacylglycerol blood leveltrolox equivalent antioxidant capacityupregulation[SDGs]SDG3journal article10.38212/2224-6614.33512-s2.0-85110287231