کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5845981 | 1128439 | 2015 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Developmental bisphenol A (BPA) exposure leads to sex-specific modification of hepatic gene expression and epigenome at birth that may exacerbate high-fat diet-induced hepatic steatosis
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کلمات کلیدی
ACOX1CEBPαSREBP1DGAT1CYBACYBBFABP1LPLPCK1BPAEndocrine disrupting chemical (EDC)NAFLDCpt1adiacylglycerol o-acyltransferase 1ASH1LEDCFFATSSPNDFAT/CD36 - FAT / CD36Free fatty acid - اسید چرب آزادfatty acid synthase - اسید چرب سنتازbisphenol A (BPA) - بیسفنول A (BPA)Bisphenol A - بیسفنول ای، بیسفنول Anon-alcoholic fatty liver disease - بیماری کبدی چربی غیر الکلیtriglyceride - تریگلیسریدpostnatal day - روز پس از زایمانtranscription start site - رونویسی شروع سایتendocrine disrupting chemical - شیمیایی خرابکار غدد درون ریزFasn - فسادLipoprotein lipase - لیپو پروتئین لیپازMethylation - متیلاسیونHistones - هیستون هاbody weight - وزن بدنSterol regulatory element binding protein 1 - پروتئین اتصال دهنده عصاره استریل 1fatty acid binding protein 1 - پروتئین مرتبط با اسید چرب 1adiposity - چاقیhigh-fat - چربی بالاcarnitine palmitoyltransferase 1a - کارنتین پالمیتیل ترانسفراز 1a
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Developmental bisphenol A (BPA) exposure increases adulthood hepatic steatosis with reduced mitochondrial function. To investigate the potential epigenetic mechanisms behind developmental BPA-induced hepatic steatosis, pregnant Sprague-Dawley rats were dosed with vehicle (oil) or BPA (100 μg/kg/day) from gestational day 6 until postnatal day (PND) 21. After weaning, offspring were either challenged with a high-fat (HF; 45% fat) or remained on a control (C) diet until PND110. From PND60 to 90, both BPA and HF diet increased the fat/lean ratio in males only, and the combination of BPA and HF diet appeared to cause the highest ratio. On PND110, Oil-HF, BPA-C, and BPA-HF males had higher hepatic lipid accumulation than Oil-C, with microvesicular steatosis being marked in the BPA-HF group. Furthermore, on PND1, BPA increased and modified hepatic triglyceride (TG) and free fatty acid (FFA) compositions in males only. In PND1 males, BPA increased hepatic expression of FFA uptake gene Fat/Cd36, and decreased the expression of TG synthesis- and β-oxidation-related genes (Dgat, Agpat6, Cebpα, Cebpβ, Pck1, Acox1, Cpt1a, Cybb). BPA altered DNA methylation and histone marks (H3Ac, H4Ac, H3Me2K4, H3Me3K36), and decreased the binding of several transcription factors (Pol II, C/EBPβ, SREBP1) within the male Cpt1a gene, the key β-oxidation enzyme. In PND1 females, BPA only increased the expression of genes involved in FFA uptake and TG synthesis (Lpl, Fasn, and Dgat). These data suggest that developmental BPA exposure alters and reprograms hepatic β-oxidation capacity in males, potentially through the epigenetic regulation of genes, and further alters the response to a HF diet.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 284, Issue 2, 15 April 2015, Pages 101-112
Journal: Toxicology and Applied Pharmacology - Volume 284, Issue 2, 15 April 2015, Pages 101-112
نویسندگان
Rita S. Strakovsky, Huan Wang, Nicki J. Engeseth, Jodi A. Flaws, William G. Helferich, Yuan-Xiang Pan, Stéphane Lezmi,