کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11026218 | 1666412 | 2018 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Biglycan gene connects metabolic dysfunction with brain disorder
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
ECMCREBORONTCHDLTrkBtropomyosin related kinase BTCAAUC - AUCBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز high-density lipoprotein - HDL یا لیپوپروتئین با دانسیته بالا یا چگالی بالاIPGTT - IPGTintraperitoneal glucose tolerance test - آزمون تحمل گلوکز داخل صفاقیTranscriptome - ترانسکریپتومOil red O - روغن قرمز OCognition - شناختBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزExtracellular matrix - ماتریکس خارج سلولیMetabolism - متابولیسم area under the curve - منطقه تحت منحنیwild type - نوع وحشیHypothalamus - هیپوتالاموسHippocampus - هیپوکامپ cAMP response element binding protein - پروتئین اتصال دهنده عنصر پاسخ cAMPtricarboxylic acid cycle - چرخه اسید تریکاربوکیلیکLiver - کبد
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Dietary fructose is a major contributor to the epidemic of diabetes and obesity, and it is an excellent model to study metabolic syndrome. Based on previous studies that Bgn gene occupies a central position in a network of genes in the brain in response to fructose consumption, we assessed the capacity of Bgn to modulate the action of fructose on brain and body. We exposed male biglycan knockout mice (Bgn0/â) to fructose for 7â¯weeks, and results showed that Bgn0/â mice compensated for a decrement in learning and memory performance when exposed to fructose. These results were consistent with an attenuation of the action of fructose on hippocampal CREB levels. Fructose also reduced the levels of CREB and BDNF in primary hippocampal neuronal cultures. Bgn siRNA treatment abolished these effects of fructose on CREB and BDNF levels, in conjunction with a reduction in a fructose-related increase in Bgn protein. In addition, fructose consumption perturbed the systemic metabolism of glucose and lipids, that were also altered in the Bgn0/ mice. Transcriptomic profiling of hypothalamus, hippocampus, and liver supported the regulatory action of Bgn on key molecular pathways involved in metabolism, immune response, and neuronal plasticity. Overall results underscore the tissue-specific role of the extracellular matrix in the regulation of metabolism and brain function, and support Bgn as a key modulator for the impact of fructose across body and brain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 12, December 2018, Pages 3679-3687
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 12, December 2018, Pages 3679-3687
نویسندگان
Zhe Ying, Hyae Ran Byun, Qingying Meng, Emily Noble, Guanglin Zhang, Xia Yang, Fernando Gomez-Pinilla,