کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10804391 | 1057265 | 2005 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The metabolic syndrome and the hepatic fatty acid drainage hypothesis
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کلمات کلیدی
CPTperoxisome-proliferator activated receptorTetradecylthioacetic acidUCPHmgVLDLLPLTTAPUFAsPPARHDLPolyunsaturated fatty acids - اسید چرب اشباع نشدهFatty acids - اسیدهای چربMetabolic syndrome - سندرم متابولیکLipoprotein lipase - لیپو پروتئین لیپازhigh density lipoprotein - لیپوپروتئین با چگالی بالاvery low density lipoprotein - لیپوپروتئین چگالی بسیار کم استlow density lipoprotein - لیپوپروتئین چگالی کمLDL - لیپوپروتئین کم چگالی(کلسترول بد)Insulin resistance - مقاومت به انسولینUncoupling protein - پروتئین جدا کردنCarnitine palmitoyltransferase - کارنتین پالمیتیل ترانسفرازGlucose - گلوکز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: The metabolic syndrome and the hepatic fatty acid drainage hypothesis The metabolic syndrome and the hepatic fatty acid drainage hypothesis](/preview/png/10804391.png)
چکیده انگلیسی
Much data indicates that lowering of plasma triglyceride levels by hypolipidemic agents is caused by a shift in the liver metabolism towards activation of peroxisome proliferator activated receptor (PPAR)α-regulated fatty acid catabolism in mitochondria. Feeding rats with lipid lowering agents leads to hypolipidemia, possibly by increased channeling of fatty acids to mitochondrial fatty acid oxidation at the expense of triglyceride synthesis. Our hypothesis is that increased hepatic fatty acid oxidation and ketogenesis drain fatty acids from blood and extrahepatic tissues and that this contributes significantly to the beneficial effects on fat mass accumulation and improved peripheral insulin sensitivity. To investigate this theory we employ modified fatty acids that change the plasma profile from atherogenic to cardioprotective. One of these novel agents, tetradecylthioacetic acid (TTA), is of particular interest due to its beneficial effects on lipid transport and utilization. These hypolipidemic effects are associated with increased fatty acid oxidation and altered energy state parameters of the liver. Experiments in PPARα-null mice have demonstrated that the effects hypolipidemic of TTA cannot be explained by altered PPARα regulation alone. TTA also activates the other PPARs (e.g., PPARδ) and this might compensate for deficiency of PPARα. Altogether, TTA-mediated clearance of blood triglycerides may result from a lowered level of apo C-III, with a subsequently induction of hepatic lipoprotein lipase activity and (re)uptake of fatty acids from very low density lipoprotein (VLDL). This is associated with an increased hepatic capacity for fatty acid oxidation, causing drainage of fatty acids from the blood stream. This can ultimately be linked to hypolipidemia, anti-adiposity, and improved insulin sensitivity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimie - Volume 87, Issue 1, January 2005, Pages 15-20
Journal: Biochimie - Volume 87, Issue 1, January 2005, Pages 15-20
نویسندگان
R.K. Berge, K.J. Tronstad, K. Berge, T.H. Rost, H. Wergedahl, O.A. Gudbrandsen, J. Skorve,