کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8258768 | 1534613 | 2018 | 38 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Short-term fructose ingestion affects the brain independently from establishment of metabolic syndrome
ترجمه فارسی عنوان
مصرف کوتاه مدت فروکتوز مغز مستقل از ایجاد سندرم متابولیک است
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کلمات کلیدی
NAFLDGLUTNeuNPGC1αcox2KHKMBPGFAPGAP 43non-alcoholic fatty liver disease - بیماری کبدی چربی غیر الکلیGlucose transporter - حمل و نقل گلوکزMetabolic syndrome - سندرم متابولیکcytochrome c oxidase subunit II - سیتوکروم C اکسیداز Subunit IIFructose - فروکتوز METS - متسionized calcium binding adaptor molecule 1 - مولکول آداپتور اتصال دهنده کلسیم یونیزه 1Mitochondria - میتوکندریاNeurons - نورون ها،یاخته های عصبیneuronal nuclei - هسته های نورونیEnergy homeostasis - هومئوستاز انرژیHippocampus - هیپوکامپ peroxisome proliferator-activated receptor gamma coactivator-1 alpha - پراکسیزوم گیرنده فعال گیرنده فعال گاما 1 آلفاGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالgrowth-associated protein 43 - پروتئین مرتبط با رشد 43Plasticity - پلاستیکketohexokinase - کتهکسوکیناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Chronic fructose ingestion is linked to the global epidemic of metabolic syndrome (MetS), and poses a serious threat to brain function. We asked whether a short period (one week) of fructose ingestion potentially insufficient to establish peripheral metabolic disorder could impact brain function. We report that the fructose treatment had no effect on liver/body weight ratio, weight gain, glucose tolerance and insulin sensitivity, was sufficient to reduce several aspects of hippocampal plasticity. Fructose consumption reduced the levels of the neuronal nuclear protein NeuN, Myelin Basic Protein, and the axonal growth-associated protein 43, concomitant with a decline in hippocampal weight. A reduction in peroxisome proliferator-activated receptor gamma coactivator-1 alpha and Cytochrome c oxidase subunit II by fructose treatment is indicative of mitochondrial dysfunction. Furthermore, the GLUT5 fructose transporter was increased in the hippocampus after fructose ingestion suggesting that fructose may facilitate its own transport to brain. Fructose elevated levels of ketohexokinase in the liver but did not affect SIRT1 levels, suggesting that fructose is metabolized in the liver, without severely affecting liver function commensurable to an absence of metabolic syndrome condition. These results advocate that a short period of fructose can influence brain plasticity without a major peripheral metabolic dysfunction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 1, January 2018, Pages 24-33
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 1, January 2018, Pages 24-33
نویسندگان
Alberto Jiménez-Maldonado, Zhe Ying, Hyae Ran Byun, Fernando Gomez-Pinilla,