کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9297731 | 1244836 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Patogenia de la hepatopatÃa grasa no alcohólica primaria
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
nonalcoholic steatohepatitis - استاتو هپاتیت غیر الکلیEsteatohepatitis no alcohólica - استاتو هپاتیت غیر الکلیNonalcoholic fatty liver disease - بیماری کبدی چربی غیر الکلیMetabolic syndrome - سندرم متابولیکSíndrome metabólico - سندرم متابولیکInsulin resistance - مقاومت به انسولینResistencia a la insulina - مقاومت به انسولینFatty liver - کبد چربHigado graso - کبد چرب
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The challenges of growing prevalence and evident trend to progressive damage of primary nonalcoholic fatty liver disease confront a poorly understood pathogenesis. It appears to develop in two steps. First, a high adipocyte protein production in the context of a silent inflammatory background causes insulin resistance in adipose tissue. It leads both to lipolysis, with increase of the circulating and hepatic uptake of free fatty acids, and hyperinsulinemia. Within hepatocytes, the subsequent lipogenesis, together with a decreased secretion of lipoproteins, induces an accumulation of excessive hepatic triglycerides (steatosis), impliying some oxidative damage, but it remain balanced by uncoupling protein upregulation and antioxidant systems activation. Second, a more forceful fat catabolism by beta and omega oxidation results in respiratory chain hyperactivity with overproduction of free radicals and reactive oxygen species that exceed the antioxidant capacity. These agents lead to hepatocellular injury and necrosis, inflammatory infiltration and fibrosis (steatohepatitis) through induction of Fas ligand and cytokines (tumor necrosis factor α, transforming growth factor β, interleukin-8), and lipid peroxidation and by-products (malondialdehyde and 4-hydroxynonenal). Other mechanisms (hepatic iron, Kupffer cells dysfunction or endotoxemia) play uncertain roles.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Medicina ClÃnica - Volume 124, Issue 17, May 2005, Pages 668-677
Journal: Medicina ClÃnica - Volume 124, Issue 17, May 2005, Pages 668-677
نویسندگان
Diego Moreno Sánchez,