کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474632 | 1550429 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Protein kinase-D1 overexpression prevents lipid-induced cardiac insulin resistance
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کلمات کلیدی
LCFAHdac5LFDBNPGSK3EFsMicroPETPKD1AMPKAMP-activated protein kinase - AMP-پروتئین کیناز فعال شده است[18F]FDG - [18F] FDGLong-chain fatty acids - اسیدهای چرب بلند زنجیره ایLeft ventricular - بطن چپElectric field stimulation - تحریک الکتریکیtriacylglycerol - تری آسیل گلیسرول TAG یا triacylglycerols - تری گلیسرید یا تری آسیل گلیسرولFatty acid transport - حمل اسید چربdiacylglycerol - دیسیل گلیسیرینanterior wall - دیواره قدامDAG - روزLow fat diet - رژیم غذایی کم چربیWestern diet - رژیم غربیSUV - ماشین شاسی بلندInsulin resistance - مقاومت به انسولینstandardized uptake value - مقدار جذب استاندارد شدهwild-type - نوع وحشیprotein kinase D - پروتئین کیناز DB-type natriuretic peptide - پپتید نیترویوتیک B نوعCardiomyopathy - کاردیومیوپاتیglucose transport - گلوکز حمل و نقلglycogen synthase kinase-3 - گلیکوزین سنتاز کیناز 3
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
In the insulin resistant heart, energy fuel selection shifts away from glucose utilization towards almost complete dependence on long-chain fatty acids (LCFA). This shift results in excessive cardiac lipid accumulation and eventually heart failure. Lipid-induced cardiomyopathy may be averted by strategies that increase glucose uptake without elevating LCFA uptake. Protein kinase-D1 (PKD1) is involved in contraction-induced glucose, but not LCFA, uptake allowing to hypothesize that this kinase is an attractive target to treat lipid-induced cardiomyopathy. For this, cardiospecific constitutively active PKD1 overexpression (caPKD1)-mice were subjected to an insulin resistance-inducing high fat-diet for 20-weeks. Substrate utilization was assessed by microPET and cardiac function by echocardiography. Cardiomyocytes were isolated for measurement of substrate uptake, lipid accumulation and insulin sensitivity. Wild-type mice on a high fat-diet displayed increased basal myocellular LCFA uptake, increased lipid deposition, greatly impaired insulin signaling, and loss of insulin-stimulated glucose and LCFA uptake, which was associated with concentric hypertrophic remodeling. The caPKD1 mice on high-fat diet showed none of these characteristics, whereas on low-fat diet a shift towards cardiac glucose utilization in combination with hypertrophy and ventricular dilation was observed. In conclusion, these data suggest that PKD pathway activation may be an attractive therapeutic strategy to mitigate lipid accumulation, insulin resistance and maladaptive remodeling in the lipid-overloaded heart, but this requires further investigation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 76, November 2014, Pages 208-217
Journal: Journal of Molecular and Cellular Cardiology - Volume 76, November 2014, Pages 208-217
نویسندگان
Ellen Dirkx, Guillaume J.J.M. van Eys, Robert W. Schwenk, Laura K.M. Steinbusch, Nicole Hoebers, Will A. Coumans, Tim Peters, Ben J. Janssen, Boudewijn Brans, Andreas T. Vogg, Dietbert Neumann, Jan F.C. Glatz, Joost J.F.P. Luiken,