کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8298939 | 1537049 | 2010 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cold tolerance of UCP1-ablated mice: A skeletal muscle mitochondria switch toward lipid oxidation with marked UCP3 up-regulation not associated with increased basal, fatty acid- or ROS-induced uncoupling or enhanced GDP effects
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کلمات کلیدی
CPTANTCOX1FCCPHNEguanosine 5'-diphosphateBSA - BSAbovine serum albumin - آلبومین سرم گاوEDTA - اتیلن دی آمین تترا استیک اسید ethylenediamine tetraacetic acid - اسید اتیلنیدین تتراستیکFatty acid - اسید چربadenine nucleotide translocase - ترانسکوز نوکلئوتید آدنینGDP - تولید ناخالص ملیCytochrome C oxidase subunit 1 - زیرسایت اکسیداز سیتوکروم C 1carnitine palmitoyl transferase - کاردینیت پالمیتویل ترانسفرازcarbonyl cyanide p-(trifluoromethoxy)phenylhydrazone - کربونیل سیانید p- (trifluoromethoxy) phenylhydrazone
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش گیاه شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Mice lacking the thermogenic mitochondrial membrane protein UCP1 (uncoupling protein 1) - and thus all heat production from brown adipose tissue - can still adapt to a cold environment (4 °C) if successively transferred to the cold. The mechanism behind this adaptation has not been clarified. To examine possible adaptive processes in the skeletal muscle, we isolated mitochondria from the hind limb muscles of cold-acclimated wild-type and UCP1(-/-) mice and examined their bioenergetic chracteristics. We observed a switch in metabolism, from carbohydrate towards lipid catabolism, and an increased total mitochondrial complement, with an increased total ATP production capacity. The UCP1(-/-) muscle mitochondria did not display a changed state-4 respiration rate (no uncoupling) and were less sensitive to the uncoupling effect of fatty acids than the wild-type mitochondria. The content of UCP3 was increased 3-4 fold, but despite this, endogenous superoxide could not invoke a higher proton leak, and the small inhibitory effect of GDP was unaltered, indicating that it was not mediated by UCP3. Double mutant mice (UCP1(-/-) plus superoxide dismutase 2-overexpression) were not more cold sensitive than UCP1(-/-), bringing into question an involvement of reactive oxygen species (ROS) in activation of any alternative thermogenic mechanism. We conclude that there is no evidence for an involvement of UCP3 in basal, fatty-acid- or superoxide-stimulated oxygen consumption or in GDP sensitivity. The adaptations observed did not imply any direct alternative process for nonshivering thermogenesis but the adaptations observed would be congruent with adaptation to chronically enhanced muscle activity caused by incessant shivering in these mice.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Bioenergetics - Volume 1797, Issues 6â7, JuneâJuly 2010, Pages 968-980
Journal: Biochimica et Biophysica Acta (BBA) - Bioenergetics - Volume 1797, Issues 6â7, JuneâJuly 2010, Pages 968-980
نویسندگان
Irina G. Shabalina, Joris Hoeks, Tatiana V. Kramarova, Patrick Schrauwen, Barbara Cannon, Jan Nedergaard,