کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10752563 | 1050328 | 2015 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Glycerol 3-phosphate dehydrogenase 1 deficiency enhances exercise capacity due to increased lipid oxidation during strenuous exercise
ترجمه فارسی عنوان
کمبود گلیسرول 3-فسفات دهیدروژناز 1 باعث افزایش توان ورزشی در اثر افزایش اکسیداسیون چربی در طول ورزش شدید
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کلمات کلیدی
AICARCOX4Gpd2cytochrome c oxidase subunit 2Cytochrome c oxidase subunit 4gpd1PGC-1 alphacox2AMPKCPTAMPAMP activated protein kinase - AMP پروتئین کیناز فعال شده استNAD+ - NAD +Adenosine Triphosphate - آدنوزین تری فسفاتATP - آدنوزین تری فسفات یا ATPadenosine monophosphate - آدنوزین مونوفسفرهoxidized nicotinamide adenine dinucleotide - اکسید نیکوتین آمید آدنین دینکلوتیدTransgenic - تراریختهHEA - سرVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)NADH - نادانperoxisome proliferator-activated receptor gamma coactivator 1 alpha - پراکسیسوم پرولاکتین گیرنده گاما گیرنده 1 آلفاCarnitine palmitoyltransferase - کارنتین پالمیتیل ترانسفرازreduced nicotinamide adenine dinucleotide - کاهش ninocotinamide adenine dinucleotideGlycerol-3-phosphate dehydrogenase 1 - گلیسرول 3-فسفات دهیدروژناز 1Glycolysis - گلیکولیز یا قندکافت
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
A large percentage of energy produced during high-intensity exercise depends on the aerobic glycolytic pathway. Maintenance of a cytoplasmic redox balance ([NADH]/[NAD+] ratio) by the glycerophosphate shuttle involves sustained aerobic glycolysis. Glycerol 3-phosphate dehydrogenase 1 (GPD1) catalyzes an oxidation reaction in the glycerophosphate shuttle. In this study, we examined whether GPD1 deficiency decreases exercise capacity due to impairment of aerobic glycolysis by using the GPD1 null mouse model BALB/cHeA (HeA). Unexpectedly, we found that exercise endurance was significantly higher in HeA mice than in BALBc/By (By) mice used as controls. Furthermore, aerobic glycolysis in HeA mice was not impaired. During exercise, lipid oxidation was significantly higher in HeA mice than in By mice, concomitant with an increase in phosphorylation of AMP-activated protein kinase (AMPK). HeA mice also showed a delay in the onset of muscle glycogen usage and lactate production during exercise. These data suggest that contribution of lipid oxidation as a fuel source for exercise is increased in HeA mice, and GPD1 deficiency enhances exercise capacity by increasing lipid oxidation, probably due to activation of AMPK. We propose that GPD1 deficiency induces an adaptation that enhances lipid availability in the skeletal muscle during exercise.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 457, Issue 4, 20 February 2015, Pages 653-658
Journal: Biochemical and Biophysical Research Communications - Volume 457, Issue 4, 20 February 2015, Pages 653-658
نویسندگان
Tomoki Sato, Akihito Morita, Nobuko Mori, Shinji Miura,