کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8301573 | 1537701 | 2016 | 36 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Knockdown of triglyceride synthesis does not enhance palmitate lipotoxicity or prevent oleate-mediated rescue in rat hepatocytes
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کلمات کلیدی
ATF3NTCUPRNAFLDDGATSFAMUFAFFAROS - ROSNon-alcoholic steatohepatitis - استئاتوهپاتیت غیرالکلیEndoplasmic reticulum stress - استرس شبکه آندوپلاسمیOleic acid - اسید اولئیکFree fatty acid - اسید چرب آزادsaturated fatty acid - اسید چرب اشباع شدهmonounsaturated fatty acid - اسید چرب غیر اشباعsaturated fatty acids - اسیدهای چرب اشباع شدهnon-alcoholic fatty liver disease - بیماری کبدی چربی غیر الکلیtriacylglycerol - تری آسیل گلیسرول Triglycerides - تریگلیسریدCHOP - تکه کردنDiacylglycerol acyltransferase - دیسیللیسرول آکیلتانسفرازازendoplasmic reticulum - شبکه آندوپلاسمی phosphatidylcholine - فسفاتیدیل کولینPhospholipid - فسفولیپیدactivating transcription factor 3 - فعال کردن عامل رونویسی 3Lipoapoptosis - لیپوآپپتوزیسPhospholipid metabolism - متابولیسم فسفولیپیدNash - نوشUnfolded protein response - پاسخ پروتئین آشکارPalmitic acid - پالمیتیک اسیدCCAAT/enhancer-binding protein homologous protein - پروتئین هموسیستون پروتئین پروتئین CCAAT / پروتئین تقویت کنندهReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Experiments in a variety of cell types, including hepatocytes, consistently demonstrate the acutely lipotoxic effects of saturated fatty acids, such as palmitate (PA), but not unsaturated fatty acids, such as oleate (OA). PAÂ +Â OA co-treatment fully prevents PA lipotoxicity through mechanisms that are not well defined but which have been previously attributed to more efficient esterification and sequestration of PA into triglycerides (TGs) when OA is abundant. However, this hypothesis has never been directly tested by experimentally modulating the relative partitioning of PA/OA between TGs and other lipid fates in hepatocytes. In this study, we found that addition of OA to PA-treated hepatocytes enhanced TG synthesis, reduced total PA uptake and PA lipid incorporation, decreased phospholipid saturation and rescued PA-induced ER stress and lipoapoptosis. Knockdown of diacylglycerol acyltransferase (DGAT), the rate-limiting step in TG synthesis, significantly reduced TG accumulation without impairing OA-mediated rescue of PA lipotoxicity. In both wild-type and DGAT-knockdown hepatocytes, OA co-treatment significantly reduced PA lipid incorporation and overall phospholipid saturation compared to PA-treated hepatocytes. These data indicate that OA's protective effects do not require increased conversion of PA into inert TGs, but instead may be due to OA's ability to compete against PA for cellular uptake and/or esterification and, thereby, normalize the composition of cellular lipids in the presence of a toxic PA load.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1861, Issue 9, Part A, September 2016, Pages 1005-1014
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1861, Issue 9, Part A, September 2016, Pages 1005-1014
نویسندگان
Alexandra K. Leamy, Clinton M. Hasenour, Robert A. Egnatchik, Irina A. Trenary, Cong-Hui Yao, Gary J. Patti, Masakazu Shiota, Jamey D. Young,