کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5508364 | 1537687 | 2017 | 31 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The overall fatty acid absorption controlled by basolateral chylomicron excretion under regulation of p-JNK1
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
DRMFATPchylomicronMAFPFABPpmapoBMTPBELCD36LPELPCIC50iPLA2βPBSApolipoprotein B - آپولیپوپروتئین Bbromoenol lactone - بروموآنول لاکتونcluster of differentiation 36 - خوشه تمایز 36Detergent-resistant membranes - غشای مقاوم در برابر مواد شویندهPhosphate buffered saline - فسفات بافر شورphosphatidylcholine - فسفاتیدیل کولینLysophosphatidylcholine - لیزوفسفاتیدیل کولینmethyl arachidonyl fluorophosphonate - متیل آراکیدونیل فلوروفسفوناتhalf-maximal inhibitory concentration - نیمه حداکثر غلظت مهاریplasma membrane fatty acid-binding protein - پروتئین اتصال دهنده اسید چرب غشاء پلاسماmicrosomal triglyceride transfer protein - پروتئین انتقال تری گلیسرید میکروسمالیFatty acid transport protein - پروتئین حمل و نقل اسید چرب
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Suppression of fatty acid absorption is one goal to fight obesity. However, the responsible molecular mechanism is poorly understood. Aim of the present study was the search for the key regulator of the overall fatty acid absorption mechanism and its pharmaceutical modulation. As experimental tool we employed the polarized human intestinal tumor derived cell line CaCo2. Here we showed that influx of fatty acids is mediated by an apical heterotetrameric plasma membrane protein complex of which the calcium-independent membrane phospholipase A2 (iPLA2Ã) is one constituent. The newly synthesized bile acid-phospholipid conjugate ursodeoxycholate-lysophosphatidylethanolamide (UDCA-LPE) blocked iPLA2Ã, which structurally disrupted the fatty acid-uptake complex. Furthermore, the inhibition of iPLA2Ã lead to reduction of cytosolic lysophosphatidylcholine (LPC) production which suppressed p-JNK1, as a central regulator of metabolism. In a concerted action low p-JNK1 levels prohibited synthesis of the members of the fatty acid uptake complex as well as of apolipoprotein B and the connected members of the basolateral vesicular chylomicron excretion machinery, thereby inhibiting cellular lipid excretion. The basolateral chylomicron release was shown to determine the overall fatty acid-absorption capacity as rate limiting step, whereas apical uptake replenishes the cellular stores, enabling continuous transcellular movement of fatty acids. In conclusion, the UDCA-LPE mediated inhibition of p-JNK1 represents a powerful tool to control intestinal absorption of fatty acids and, thus may be employed as a drug to treat obesity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1862, Issue 9, September 2017, Pages 917-928
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1862, Issue 9, September 2017, Pages 917-928
نویسندگان
Wolfgang Stremmel, Simone Staffer, Andreas Wannhoff, Anita Pathil,