Stimulating lipolysis in subcutaneous adipose tissues by chronic dexamethasone administration in goats

•Chronic dexmethasone exposure induces lipolysis in adipose tissue of goats.•Dexmethasone stimulated lipolysis via up-regulating HSL and p-HSL protein.•The up-regulation of genes involved in the lipogenic process may indicate a compensatory feedback mechanism to maintain homeostasis, targeting the b...

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Published inLivestock science Vol. 214; pp. 62 - 67
Main Authors Hua, Canfeng, Geng, Yali, Niu, Liqiong, Chen, Qu, Cai, Liuping, Tao, Shiyu, Ni, Yingdong, Zhao, Ruqian
Format Journal Article
LanguageEnglish
Published Elsevier B.V 01.08.2018
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Summary:•Chronic dexmethasone exposure induces lipolysis in adipose tissue of goats.•Dexmethasone stimulated lipolysis via up-regulating HSL and p-HSL protein.•The up-regulation of genes involved in the lipogenic process may indicate a compensatory feedback mechanism to maintain homeostasis, targeting the balance in lipolysis induced by Dex in goats. The objective of this study was to investigate the effects of chronic stress induced by a low dosage of dexamethasone (Dex) on the lipolytic response in adipose tissue of goats. Ten male goats were randomly assigned to two groups; one group was injected subcutaneously with 0.2 mg/kg Dex, and the other group was injected subcutaneously with the same volume of saline as a control (Con) for 21 days. The result revealed that plasma triglycerides (TG) (P < 0.05) concentrations decreased in response to Dex administration. Plasma glycerol, mainly derived from degradation of TG, increased during the Dex treatment (P < 0.05). Expression of genes involved in lipolysis—including G protein β subunit (Gnb1) (P < 0.01), hormone-sensitive lipase (Lipe) (P < 0.05), and perilipin-3 (Plin3) (P < 0.05) — were up-regulated in adipose tissue by Dex. Paralleling the increase in gene expression, the pLIPE/LIPE ratio also increased in response to Dex, which reflected higher LIPE activity, in adipose tissue (P < 0.05). However, the expression of genes involved in fatty acids synthesis—such as acetyl CoA carboxylase (Acc), fatty acid synthase (Fas), and stearoyl-CoA desaturase (Scd)—were not changed by Dex, while the abundance of diglyceride acyltransferase 1 and 2 (Dgat1 and Dgat2) mRNA, which catalyze the formation of TGs from diacylglycerol and Acyl-CoA, increased (P < 0.05) in adipose tissue of Dex-treated goats compared with Con goats. Moreover, plasma leptin concentration decreased in response to Dex; however, Leptin mRNA expression tended to increase in adipose tissue, indicating a negative feedback regulatory mechanism. Adiponectin gene expression was also up-regulated in adipose tissue by Dex (P < 0.05). Taken together, our findings demonstrate that chronic glucocorticoid administration induces an imbalance in TG metabolism, resulting in a lower level of leptin and a higher level of glycerol in blood by promoting lipolysis and Gnb1 and Plin3 expression in adipose tissue, as well as increasing the pLIPE: LIPE ratio.
ISSN:1871-1413
1878-0490
DOI:10.1016/j.livsci.2018.05.020