کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1949726 | 1537783 | 2009 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A pan-PPAR ligand induces hepatic fatty acid oxidation in PPARαâ/â mice possibly through PGC-1 mediated PPARδ coactivation
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کلمات کلیدی
RT-PCRTetradecylthioacetic acidLXXLLHypolipidemicAcyl-coenzyme A synthetaseacyl-CoA oxidasePGC-1TTAPPARAF-2SRCACOACSacyl-CoA synthetase - Acyl-CoA SynthetasePPRE - ارسالactivation function-2 - تابع فعال سازی 2peroxisome proliferator-activated receptor response element - عنصر پاسخ گیرنده فعال پرولیفراسیون فعالreverse transcriptase polymerase chain reaction - واکنش زنجیره ای پلی مراز ترانس کریتاز معکوسsteroid receptor coactivator - گیرنده استروئید گیرندهperoxisome proliferator-activated receptor - گیرنده فعال فعال پروکسیومPeroxisome proliferator-activated receptors - گیرنده فعال فعال پروکسیوم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: A pan-PPAR ligand induces hepatic fatty acid oxidation in PPARαâ/â mice possibly through PGC-1 mediated PPARδ coactivation A pan-PPAR ligand induces hepatic fatty acid oxidation in PPARαâ/â mice possibly through PGC-1 mediated PPARδ coactivation](/preview/png/1949726.png)
چکیده انگلیسی
Tetradecylthioacetic acid (TTA) is a hypolipidemic modified fatty acid and a peroxisome proliferator-activated receptor (PPAR) ligand. The mechanisms of TTA-mediated effects seem to involve the PPARs, but the effects have not been assigned to any specific PPAR subtype. PPARαâ/â mice were employed to study the role of PPARα after TTA treatment. We also performed in vitro transfection assays to obtain mechanistic knowledge of how TTA affected PPAR activation in the presence of PPARγ coactivator (PGC)-1 and steroid receptor coactivators (SRC)-1 and SRC-2, which are associated with energy balance and mitochondrial biogenesis. We show that TTA increases hepatic fatty acid β-oxidation in PPARαâ/â mice. TTA acts as a pan-PPAR ligand in vitro, and PGC-1, SRC-1 and SRC-2 have cell type and PPAR-specific effects together with TTA. In the absence of exogenous ligands, SRC-1 did not induce PPAR activity, while PGC-1 was the most potent PPAR coactivator. When the coactivators were overexpressed, pronounced effects of TTA were observed especially for PPARδ and PPARγ. We conclude that PPARα is involved in, but not required for, the hypolipidemic mechanisms of TTA. It appears that the activity of PPARδ, with substantial contribution of nuclear receptor coactivators, PGC-1 in special, is conducive to TTA's mechanism of action.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1791, Issue 11, November 2009, Pages 1076-1083
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1791, Issue 11, November 2009, Pages 1076-1083
نویسندگان
Therese H. Røst, Line L. Haugan Moi, Kjetil Berge, Bart Staels, Gunnar Mellgren, Rolf K. Berge,