کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5508538 | 1537697 | 2016 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Stearoyl-CoA desaturase 1 deficiency reduces lipid accumulation in the heart by activating lipolysis independently of peroxisome proliferator-activated receptor α
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کلمات کلیدی
GAPDHG0S2FATP1acyl-CoA oxidaseCPT1ACOAMPKFFAFASACC5′-adenosine monophosphate-activated protein kinase - 5'-آدنوزین مونوفسفات فعال پروتئین کینازBSA - BSAbovine serum albumin - آلبومین سرم گاوAtgl - اتگلacetyl-CoA carboxylase - استیل کروکسی سیلازFatty acid - اسید چربfatty acid synthase - اسید چرب سنتازdiacylglycerol - دیسیل گلیسیرینDAG - روزadipose triglyceride lipase - لیپاز تری گلیسیرید چربیfatty acid transport protein 1 - پروتئین حمل و نقل اسید چرب 1Carnitine palmitoyltransferase 1 - کارنتین پالمیتویل ترانسفراز 1glyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Stearoyl-CoA desaturase 1 (SCD1) has recently been shown to be a critical control point in the regulation of cardiac metabolism and function. Peroxisome proliferator-activated receptor α (PPARα) is an important regulator of myocardial fatty acid uptake and utilization. The present study used SCD1 and PPARα double knockout (SCD1â/â/PPARαâ/â) mice to test the hypothesis that PPARα is involved in metabolic changes in the heart that are caused by SCD1 downregulation/inhibition. SCD1 deficiency decreased the intracellular content of free fatty acids, triglycerides, and ceramide in the heart of SCD1â/â and SCD1â/â/PPARαâ/â mice. SCD1 ablation in PPARαâ/â mice decreased diacylglycerol content in cardiomyocytes. These results indicate that the reduction of fat accumulation in the heart associated with SCD1 deficiency occurs independently of the PPARα pathway. To elucidate the mechanism of the observed changes, we treated HL-1 cardiomyocytes with the SCD1 inhibitor A939572 and/or PPARα inhibitor GW6471. SCD1 inhibition decreased the level of lipogenic proteins and increased lipolysis, reflected by a decrease in the content of adipose triglyceride lipase inhibitor G0S2 and a decrease in the ratio of phosphorylated hormone-sensitive lipase (HSL) at Ser565 to HSL (pHSL[Ser565]/HSL). PPARα inhibition alone did not affect the aforementioned protein levels. Finally, PPARα inhibition decreased the phosphorylation level of 5â²-adenosine monophosphate-activated protein kinase, indicating lower mitochondrial fatty acid oxidation. In summary, SCD1 ablation/inhibition decreased cardiac lipid content independently of the action of PPARα by reducing lipogenesis and activating lipolysis. The present data suggest that SCD1 is an important component in maintaining proper cardiac lipid metabolism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1861, Issue 12, Part A, December 2016, Pages 2029-2037
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1861, Issue 12, Part A, December 2016, Pages 2029-2037
نویسندگان
Tomasz Bednarski, Adam Olichwier, Agnieszka Opasinska, Aleksandra Pyrkowska, Ana-Maria Gan, James M. Ntambi, Pawel Dobrzyn,