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

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 characte...

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Published inAnimal cells and systems Vol. 24; no. 3; pp. 151 - 159
Main Authors Jang, Hyung Seok, Kim, Kyeongdae, Lee, Mi-Ran, Kim, Shin-Hye, Choi, Jae-Hoon, Park, Mi Jung
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 03.05.2020
Taylor & Francis Ltd
Taylor & Francis Group
한국통합생물학회
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ISSN1976-8354
2151-2485
2151-2485
DOI10.1080/19768354.2020.1778080

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Summary: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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ISSN:1976-8354
2151-2485
2151-2485
DOI:10.1080/19768354.2020.1778080