کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9886557 | 1537835 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Deficiency of PPARα disturbs the response of lipogenic flux and of lipogenic and cholesterogenic gene expression to dietary cholesterol in mouse white adipose tissue
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کلمات کلیدی
ACCTAGFASliver-X receptorPPARSREBPPPARαHMG-CoANEFALXR3-hydroxy-3-methylglutaryl coenzyme A - 3 هیدروکسی 3-متیل گلوتاریل کوآنزیم Aacetyl coA carboxylase - استیل کولا کربوکسیلازfatty acid synthase - اسید چرب سنتازNon-esterified fatty acid - اسید چرب غیر استرادیلیAdipose tissue - بافت چربیmRNA expression - بیان mRNAtriacylglycerol - تری آسیل گلیسرول Low-density lipoprotein - لیپوپروتئین کم چگالی یا الدیال LDL - لیپوپروتئین کم چگالی(کلسترول بد)cholesterol - کلسترولperoxisome proliferator-activated receptor - گیرنده فعال فعال پروکسیوم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
PPARα-deficiency in mice fed a high-carbohydrate, low-cholesterol diet was associated with a decreased weight of epididymal adipose tissue and an increased concentration of adipose tissue cholesterol. Consumption of a high (2% w/w) cholesterol diet resulted in a further increase in the concentration of cholesterol and a further decrease in epididymal fat pad weight in PPARα-null mice, but had no effect in the wild-type. These reductions in fat pad weight were associated with an increase in hepatic triacylglycerol content, indicating that both PPARα-deficiency and cholesterol altered the distribution of triacylglycerol in the body. Adipose tissue de novo lipogenesis was increased in PPARα-null mice and was further enhanced when they were fed a cholesterol-rich diet; no such effect was observed in the wild-type mice. The increased lipogenesis in the chow-fed PPARα-null mice was accompanied paradoxically by lower mRNA expression of SREBP-1c and its target genes, acetyl-CoA carboxylase and fatty acid synthase. Consumption of a high-cholesterol diet increased the mRNA expression of these genes in the PPARα-deficient mice but not in the wild-type. De novo cholesterol synthesis was not detectable in the adipose tissue of either genotype despite a relatively high expression of the mRNA's encoding SREBP-2 and 3-hydroxy-3-methylglutaryl Coenzyme A reductase. The mRNA expression of these genes and of the LDL-receptor in adipose tissue of the PPARα-deficient mice was lower than that of the wild-type and was not downregulated by cholesterol feeding. The results suggest that PPARα plays a role in adipose tissue cholesterol and triacylglycerol homeostasis and prevents cholesterol-mediated changes in de novo lipogenesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1734, Issue 3, 1 June 2005, Pages 259-268
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1734, Issue 3, 1 June 2005, Pages 259-268
نویسندگان
K.K. Islam, B.L. Knight, K.N. Frayn, D.D. Patel, G.F. Gibbons,