首頁> 外文期刊>Biochimica et Biophysica Acta. Molecular and cell biology of Lipids >Insulin, glucagon and fatty acid treatment of hepatocytes does not result in phosphorylation or changes in activity of triacylglycerol hydrolase
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Insulin, glucagon and fatty acid treatment of hepatocytes does not result in phosphorylation or changes in activity of triacylglycerol hydrolase

機譯:胰島素,胰高血糖素和脂肪酸對肝細胞的處理不會導致磷酸化或三?;视退饷富钚缘淖兓?

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摘要

It is recognized that the majority of very low density lipoprotein (VLDL) associated triacylglycerol (TG) is synthesized from fatty acids and partial acylglycerols generated by lipolysis of intra-hepatic storage rather than made de novo. Triacylglycerol hydrolase (TGH) is involved in mobilizing stored TG. Modulating the ability of TGH to hydrolyze stored lipids represents a potentially regulated and rate limiting step in VLDL assembly. Phosphorylation of lipases and carboxylesterases trigger diverse but functionally significant events. We explored the potential for regulating the mobilization of hepatic TG through phosphorylation of TGH. Insulin is known to suppress VLDL secretion from liver, and glucagon can be considered an opposing hormone. However, neither insulin nor glucagon treatment of hepatocytes led to phosphorylation of TGH or changes in its activity. Augmenting intracellular TG stores by incubations with oleic acid also did not lead to changes in TGH activity. Therefore, changes in phosphorylation state are not a mechanism for regulating TGH activity, access to TG substrate pools or for TGH-mediated contributions to VLDL assembly and secretion. (c) 2005 Elsevier B.V All rights reserved.
機譯:公認的是,大多數非常低密度脂蛋白(VLDL)相關的三?;视停═G)是由通過肝內存儲脂解產生的脂肪酸和部分?;视秃铣傻?,而不是從頭合成的。三?;视退饷福═GH)參與動員存儲的TG。調節TGH水解儲存的脂質的能力代表了VLDL組裝中潛在的受調控和限速步驟。脂肪酶和羧酸酯酶的磷酸化會引發多種多樣的但功能上重要的事件。我們探索了通過TGH磷酸化來調節肝TG動員的潛力。已知胰島素可以抑制肝臟中VLDL的分泌,而胰高血糖素可以被認為是一種相反的激素。但是,胰島素和胰高血糖素對肝細胞的處理均不會導致TGH磷酸化或改變其活性。通過與油酸孵育來增強細胞內TG的儲存也不會導致TGH活性的改變。因此,磷酸化狀態的變化不是調節TGH活性,進入TG底物池或TGH介導的VLDL組裝和分泌的機制。 (c)2005 Elsevier B.V保留所有權利。

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