کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10756438 | 1050383 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The role of glycerol-3-phosphate dehydrogenase 1 in the progression of fatty liver after acute ethanol administration in mice
ترجمه فارسی عنوان
نقش گلیسرول 3-فسفات دهیدروژناز 1 در پیشرفت کبد چرب بعد از تزریق حاد اتانول در موش
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کلمات کلیدی
PPARGyKDGATChREBPSREBP-1cPEPCKacyl-CoA:diacylglycerol acyltransferasePGC-1 alphagpd1PYGLFOXO1DHAPGAPDHFASNADPHcarbohydrate response element-binding proteinNAD+ - NAD +fatty acid synthase - اسید چرب سنتازoxidized nicotinamide adenine dinucleotide - اکسید نیکوتین آمید آدنین دینکلوتیدtriglyceride - تریگلیسریدForkhead box O1 - جعبه O1 جعبهTriglyceride synthesis - سنتز تری گلیسریدphosphoenolpyruvate carboxykinase - فسفوآنولپیرود کربوکسیکینازLipogenesis - لیپوژنزNADH - نادانnicotinamide adenine dinucleotide phosphate - نیکوتین آمید adenine dinucleotide phosphateperoxisome proliferator-activated receptor gamma coactivator 1 alpha - پراکسیسوم پرولاکتین گیرنده گاما گیرنده 1 آلفاsterol regulatory element-binding protein-1c - پروتئین وابسته به استرول تنظیم کننده پروتئین-1creduced nicotinamide adenine dinucleotide - کاهش ninocotinamide adenine dinucleotideglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژنازglycerol-3-phosphate - گلیسرول 3-فسفاتGlycerol-3-phosphate dehydrogenase 1 - گلیسرول 3-فسفات دهیدروژناز 1Glycerol kinase - گلیسرول کینازGlyceroneogenesis - گلیسیرینوژنزperoxisome proliferator-activated receptor - گیرنده فعال فعال پروکسیوم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
Acute ethanol consumption leads to the accumulation of triglycerides (TGs) in hepatocytes. The increase in lipogenesis and reduction of fatty acid oxidation are implicated as the mechanisms underlying ethanol-induced hepatic TG accumulation. Although glycerol-3-phosphate (Gro3P), formed by glycerol kinase (GYK) or glycerol-3-phosphate dehydrogenase 1 (GPD1), is also required for TG synthesis, the roles of GYK and GPD1 have been the subject of some debate. In this study, we examine (1) the expression of genes involved in Gro3P production in the liver of C57BL/6J mice in the context of hepatic TG accumulation after acute ethanol intake, and (2) the role of GPD1 in the progression of ethanol-induced fatty liver using GPD1 null mice. As a result, in C57BL/6J mice, ethanol-induced hepatic TG accumulation began within 2Â h and was 1.7-fold greater than that observed in the control group after 6Â h. The up-regulation of GPD1 began 2Â h after administering ethanol, and significantly increased 6Â h later with the concomitant escalation in the glycolytic gene expression. The incorporation of 14C-labelled glucose into TG glycerol moieties increased during the same period. On the other hand, in GPD1 null mice carrying normal GYK activity, no significant increase in hepatic TG level was observed after acute ethanol intake. In conclusion, GPD1 and glycolytic gene expression is up-regulated by ethanol, and GPD1-mediated incorporation of glucose into TG glycerol moieties together with increased lipogenesis, is suggested to play an important role in ethanol-induced hepatic TG accumulation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 444, Issue 4, 21 February 2014, Pages 525-530
Journal: Biochemical and Biophysical Research Communications - Volume 444, Issue 4, 21 February 2014, Pages 525-530
نویسندگان
Tomoki Sato, Akihito Morita, Nobuko Mori, Shinji Miura,