کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11007582 | 1540606 | 2018 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Long-term exposure to high-sucrose diet down-regulates hepatic endoplasmic reticulum-stress adaptive pathways and potentiates de novo lipogenesis in weaned male mice
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کلمات کلیدی
ATF6inositol-requiring enzyme 1 alphaCPT-1αstearoyl-CoA desaturase-1SCD1ChREBPGRP78SREBP-1cNrf2GAPDHPPARαC/EBP-homologous protein - C / EBP-homologous proteinIRE1α - IRE1aperoxisome proliferator-activated receptor alpha - آلفای گیرنده پرولیفراتور فعال فعالde novo lipogenesis - از لیپوژنز جدیدMicrovesicular steatosis - استئاتوز میکروزیکولارEndoplasmic reticulum stress - استرس شبکه آندوپلاسمیfatty acid synthase - اسید چرب سنتازNonalcoholic fatty liver disease - بیماری کبدی چربی غیر الکلیCHOP - تکه کردنhigh-sucrose diet - رژیم غذایی بالا ساکارزMetabolic syndrome - سندرم متابولیکFasn - فسادactivating transcription factor 6 - فعال کردن عامل رونویسی 6sterol regulatory element-binding protein 1c - پروتئین وابسته به استرول تنظیم کننده پروتئین 1cprotein kinase RNA-like ER kinase - پروتئین کیناز RNA مانند ER kinasePERK - پرکcarnitine palmitoyltransferase 1α - کارنتین پالمیتیل ترانسفراز 1αcarbohydrate-responsive element-binding protein - کربوهیدرات پاسخ دهنده پروتئین اتصال دهندهglucose regulated protein 78 - گلوکز پروتئین تنظیم شده 78glyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Childhood consumption of added sugars, such as sucrose, has been associated to increased risk of metabolic syndrome (MetS) and nonalcoholic fatty liver disease (NAFLD). Although the mechanisms underlying NAFLD onset are incompletely defined, recent evidence has proposed a role for the endoplasmic reticulum (ER) stress. Thus, the present study sought to investigate the metabolic outcomes of high-sucrose intake on weaned Swiss mice fed a 25% sucrose diet for 30, 60 and 90 days in comparison to regular chow-fed controls. High-sucrose feeding promoted progressive metabolic and oxidative disturbances, starting from fasting and fed hyperglycemia, hyperinsulinemia, glucose intolerance and increased adiposity at 30-days; passing by insulin resistance, hypertriglyceridemia and NAFLD onset at 60 days; until late hepatic oxidative damage at 90 days. In parallel, assessment of transcriptional and/or translational levels of de novo lipogenesis (DNL) and ER stress markers showed up-regulation of both fatty acid synthesis (ChREBP and SCD1) and oxidation (PPARα and CPT-1α), as well as overexpression of unfolded protein response sensors (IRE1α, PERK and ATF6), chaperones (GRP78 and PDIA1) and antioxidant defense (NRF2) genes at 30 days. At 60 days, fatty acid oxidation genes were down-regulated, and ER stress switched over toward a proapoptotic pattern via up-regulation of BAK protein and CHOP gene levels. Finally, down-regulation of both NRF2 and CPT-1α protein levels led to late up-regulation of SREBP-1c and exponential raise of fatty acids synthesis. In conclusion, our study originally demonstrates a temporal relationship between DNL and ER stress pathways toward MetS and NAFLD development on weaned rats fed a high-sucrose diet.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Nutritional Biochemistry - Volume 62, December 2018, Pages 155-166
Journal: The Journal of Nutritional Biochemistry - Volume 62, December 2018, Pages 155-166
نویسندگان
Karla Frida Torres Flister, Bruno Araújo Serra Pinto, Lucas Martins França, Caio Fernando Ferreira Coêlho, Pâmela Costa dos Santos, Caroline Castro Vale, Daniela Kajihara, Victor Debbas, Francisco Rafael Martins Laurindo,