کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8336786 | 1540643 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Diets rich in fructose, fat or fructose and fat alter intestinal barrier function and lead to the development of nonalcoholic fatty liver disease over time
ترجمه فارسی عنوان
رژیم های غذایی غنی از فروکتوز، چربی یا فروکتوز و چربی بدن را تقویت عملکرد مانع روده و منجر به توسعه بیماری های غیر کلامی کبد چرب در طول زمان
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کلمات کلیدی
TLR-4NAFLDARG-1ZO-1IRS-1TNFαNASMCP-14-HNEiNOS4-hydroxynonenalMYD88ALTarginase 1 - آرژیناز 1alanine-aminotransferase - آلانین آمینوترانسفرازTight junction - اتصال تنگnonalcoholic steatohepatitis - استاتو هپاتیت غیر الکلیEndotoxin - اندوتوکسینNonalcoholic fatty liver disease - بیماری کبدی چربی غیر الکلیtumor necrosis factor α - تومور نکروز عامل αinsulin receptor substrate 1 - زیر بغل گیرنده انسولین 1Aging - سالخوردگیinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییzonula occludens 1 - شل و بسته 1Macronutrients - مغذی هاNAFLD activity score - نمره فعالیت NAFLDNash - نوشmyeloid differentiation primary response gene 88 - پاسخ اولیه ژن 88، اختلال میلوئیدmonocyte chemotactic protein 1 - پروتئین chemotactic monocyte 1insulin receptor - گیرنده انسولینToll-like receptor 4 - گیرنده تله مانند 4
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
General overnutrition but also a diet rich in certain macronutrients, age, insulin resistance and an impaired intestinal barrier function may be critical factors in the development of nonalcoholic fatty liver disease (NAFLD). Here the effect of chronic intake of diets rich in different macronutrients, i.e. fructose and/or fat on liver status in mice, was studied over time. C57BL/6J mice were fed plain water, 30% fructose solution, a high-fat diet or a combination of both for 8 and 16 weeks. Indices of liver damage, toll-like receptor 4 (TLR-4) signaling cascade, macrophage polarization and insulin resistance in the liver and intestinal barrier function were analyzed. Chronic exposure to a diet rich in fructose and/or fat was associated with the development of hepatic steatosis that progressed with time to steatohepatitis in mice fed a combination of macronutrients. The development of NAFLD was also associated with a marked reduction of the mRNA expression of insulin receptor, whereas hepatic expressions of TLR-4, myeloid differentiation primary response gene 88 and markers of M1 polarization of macrophages were induced in comparison to controls. Bacterial endotoxin levels in portal plasma were found to be increased while levels of the tight junction protein occludin and zonula occludens 1 were found to be significantly lower in the duodenum of all treated groups after 8 and 16 weeks. Our data suggest that chronic intake of fructose and/or fat may lead to the development of NAFLD over time and that this is associated with an increased translocation of bacterial endotoxin.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Nutritional Biochemistry - Volume 26, Issue 11, November 2015, Pages 1183-1192
Journal: The Journal of Nutritional Biochemistry - Volume 26, Issue 11, November 2015, Pages 1183-1192
نویسندگان
Cathrin Sellmann, Josephine Priebs, Marianne Landmann, Christian Degen, Anna Janina Engstler, Cheng Jun Jin, Stefanie Gärttner, Astrid Spruss, Otmar Huber, Ina Bergheim,