کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9886499 | 1537829 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Insulin, glucagon and fatty acid treatment of hepatocytes does not result in phosphorylation or changes in activity of triacylglycerol hydrolase
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کلمات کلیدی
DMEMFBSBSDLHSLBSA - BSADulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده Dulbeccobovine serum albumin - آلبومین سرم گاوapo - آپوapolipoprotein - آپولیپوپروتئینAtgl - اتگلImmunoprecipitation - تخریب ایمنیMUH - خیلی ممنونhorse serum - سرب اسبfetal bovine serum - سرم جنین گاوendoplasmic reticulum - شبکه آندوپلاسمی adipose triglyceride lipase - لیپاز تری گلیسیرید چربیhormone sensitive lipase - لیپاز حساس به هورمونbile salt-dependent lipase - لیپاز وابسته به نمک صفراmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenMAP kinase - کیناز MAP
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Insulin, glucagon and fatty acid treatment of hepatocytes does not result in phosphorylation or changes in activity of triacylglycerol hydrolase Insulin, glucagon and fatty acid treatment of hepatocytes does not result in phosphorylation or changes in activity of triacylglycerol hydrolase](/preview/png/9886499.png)
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1736, Issue 3, 1 October 2005, Pages 189-199
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1736, Issue 3, 1 October 2005, Pages 189-199
نویسندگان
Dean Gilham, Kathleen R. Perreault, Charles F.B. Holmes, David N. Brindley, Dennis E. Vance, Richard Lehner,