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Treatment of growth hormone attenuates hepatic steatosis in hyperlipidemic mice via downregulation of hepatic CD36 expressionopen access

Authors
Jang, Hyung SeokKim, KyeongdaeLee, Mi-RanKim, Shin-HyeChoi, Jae-HoonPark, Mi Jung
Issue Date
May-2020
Publisher
TAYLOR & FRANCIS LTD
Keywords
Growth hormone; hyperlipidemia; hepatic steatosis; atherosclerosis; CD36
Citation
ANIMAL CELLS AND SYSTEMS, v.24, no.3, pp.151 - 159
Indexed
SCIE
SCOPUS
KCI
Journal Title
ANIMAL CELLS AND SYSTEMS
Volume
24
Number
3
Start Page
151
End Page
159
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/1933
DOI
10.1080/19768354.2020.1778080
ISSN
1976-8354
Abstract
The recombinant human growth hormone (GH) has been used for the treatment of growth hormone deficiency (GHD) and diverse short stature state, and its physiological and therapeutic effects are well documented. However, since the effect of GH treatment on metabolic disorders has not been well characterized, we injected GH to Western diet-fed low-density lipoprotein receptor-deficient (Ldlr−/−) mice to understand the exact effect of GH on metabolic diseases including atherosclerosis, hepatic steatosis, and obesity. Exogenous GH treatment increased plasma IGF-1 concentration and decreased body weight without affecting serum lipid profiles. GH treatment changed neither atherosclerotic lesion size nor collagen and smooth muscle cells accumulation in the lesion. GH treatment reduced macrophage accumulation in adipose tissue. Importantly, GH treatment attenuated hepatic steatosis and inflammation. The hepatic expression IL-1β mRNA were decreased by GH treatment. The mRNA and protein levels of CD36 were markedly decreased in GH treated mice without significant changes in other molecules related to lipid metabolism. Therefore, the treatment of GH treatment could attenuate hepatic steatosis and inflammation with downregulation of CD36 expression in hyperlipidemic condition.
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