کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474422 | 1550426 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Impaired cytosolic NADH shuttling and elevated UCP3 contribute to inefficient citric acid cycle flux support of postischemic cardiac work in diabetic hearts
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کلمات کلیدی
UCP3CACMVO2OMCrPPLCFADM2UCP2nuclear magnetic resonance - رزونانس مغناطیسی هستهایdb/db Mouse - db / db mouselong chain fatty acid - اسید چرب زنجیره طولانیFatty acid oxidation - اکسیداسیون اسید چربischemia/reperfusion - ایسکمی / رپرفیوژنNMR - تشدید مغناطیسی هستهای db/db - دبی / دسی بلType 2 diabetes mellitus - دیابت نوع دوMalate–aspartate shuttle - شاتل مالتا-آسپارتاتFAO - فائوmyocardial oxygen consumption - مصرف اکسیژن قلبRate pressure product - مقدار فشار محصولMitochondria - میتوکندریاNorm - نورمuncoupling protein 2 - پروتئین جدا سازی 2Uncoupling protein 3 - پروتئین جدا سازی 3Uncoupling protein - پروتئین جدا کردنCitric acid cycle - چرخه اسید سیتریکreducing equivalents - کاهش معادل
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Diabetic hearts are subject to more extensive ischemia/reperfusion (ISC/REP) damage. This study examined the efficiency of citric acid cycle (CAC) flux and the transfer of cytosolic reducing equivalents into the mitochondria for oxidative support of cardiac work following ISC/REP in hearts of c57bl/6 (NORM) and type 2 diabetic, db/db mouse hearts. Flux through the CAC and malate-aspartate shuttle (MA) were monitored via dynamic 13C NMR of isolated hearts perfused with 13C palmitate + glucose. MA flux was lower in db/db than NORM. Oxoglutarate malate carrier (OMC) was elevated in the db/db heart, suggesting a compensatory response to low NADHc. Baseline CAC flux per unit work (rate-pressure-product, RPP) was similar between NORM and db/db, but ISC/REP reduced the efficiency of CAC flux/RPP by 20% in db/db. ISC/REP also increased UCP3 transcription, indicating potential for greater uncoupling. Therefore, ISC/REP induces inefficient carbon utilization through the CAC in hearts of diabetic mice due to the combined inefficiencies in NADHc transfer per OMC content and increased uncoupling via UCP3. Ischemia and reperfusion exacerbated pre-existing mitochondrial defects and metabolic limitations in the cytosol of diabetic hearts. These limitations and defects render diabetic hearts more susceptible to inefficient carbon fuel utilization for oxidative energy metabolism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 79, February 2015, Pages 13-20
Journal: Journal of Molecular and Cellular Cardiology - Volume 79, February 2015, Pages 13-20
نویسندگان
Natasha H. Banke, E. Douglas Lewandowski,