کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8302396 | 1537731 | 2014 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Liquid fructose downregulates Sirt1 expression and activity and impairs the oxidation of fatty acids in rat and human liver cells
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کلمات کلیدی
Sirt1Forkhead box protein A2sterol response element binding protein 1GPAT1L-PKCYP4A1SREBP1HNF4SCD1FOXA2ChREBPT2DMsirtuin 1NAMPTAMPKACCPPARαTSAPP2AAPRTACOPGC-1αFASAMP-activated protein kinase - AMP-پروتئین کیناز فعال شده استStearoyl-CoA desaturase 1 - استارویل-کاپا دساتوراز 1fatty acid synthase - اسید چرب سنتازTrichostatin A - تریکوستاتین Atriglyceride - تریگلیسریدSteatosis - تغییر چرب یا استئاتوز Type 2 diabetes mellitus - دیابت نوع دوHepatic Nuclear Factor 4 - فاکتور هسته ای کبدی 4nicotinamide phosphoribosyltransferase - نیکوتین آمید فسفریبوسیل ترانسفرازcarbohydrate response element binding protein - پروتئین اتصال دهنده عنصر پاسخ کربوهیدراتGlucokinase - گلوکوکینازPeroxisome proliferator activated receptor α - گیرنده پروتئینزای پروکسیوم فعال α
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Fructose ingestion is associated with the production of hepatic steatosis and hypertriglyceridemia. For fructose to attain these effects in rats, simultaneous induction of fatty acid synthesis and inhibition of fatty acid oxidation is required. We aimed to determine the mechanism involved in the inhibition of fatty acid oxidation by fructose and whether this effect occurs also in human liver cells. Female rats were supplemented or not with liquid fructose (10% w/v) for 7 or 14 days; rat (FaO) and human (HepG2) hepatoma cells, and human hepatocytes were incubated with fructose 25 mM for 24 h. The expression and activity of the enzymes and transcription factors relating to fatty acid β-oxidation were evaluated. Fructose inhibited the activity of fatty acid β-oxidation only in livers of 14-day fructose-supplemented rats, as well as the expression and activity of peroxisome proliferator activated receptor α (PPARα). Similar results were observed in FaO and HepG2 cells and human hepatocytes. PPARα downregulation was not due to an osmotic effect or to an increase in protein-phosphatase 2A activity caused by fructose. Rather, it was related to increased content in liver of inactive and acetylated peroxisome proliferator activated receptor gamma coactivator 1α, due to a reduction in sirtuin 1 expression and activity. In conclusion, fructose inhibits liver fatty acid oxidation by reducing PPARα expression and activity, both in rat and human liver cells, by a mechanism involving sirtuin 1 down-regulation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1841, Issue 4, April 2014, Pages 514-524
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1841, Issue 4, April 2014, Pages 514-524
نویسندگان
Alba Rebollo, Núria Roglans, Miguel Baena, Rosa M. Sánchez, Manel Merlos, Marta Alegret, Juan C. Laguna,