کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8259899 | 1534647 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Reduced nuclear protein 1 expression improves insulin sensitivity and protects against diet-induced glucose intolerance through up-regulation of heat shock protein 70
ترجمه فارسی عنوان
کاهش بیان پروتئین هسته ای 1 حساسیت انسولین را بهبود می بخشد و در برابر عدم تحمل گلوکز ناشی از رژیم غذایی از طریق تنظیم مقررات پروتئین شوک حرارت 70 محافظت می کند
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کلمات کلیدی
HFDHOMA-IRhsp70T2DHSF-1NFDHomeostasis model assessment-insulin resistance - ارزیابی مدل Homostasis - مقاومت به انسولینIslets of Langerhans - جزایر لانگرهانسType 2 diabetes - دیابت نوع 2High fat diet - رژیم غذایی با چربی بالاHeat shock transcription factor 1 - فاکتور رونویسی شوک حرارت 1Insulin resistance - مقاومت به انسولینGlucose homeostasis - هوموستاز گلوکزHeat shock protein - پروتئین شوک حرارتheat shock protein 70 - پروتئین شوک حرارت 70
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
We recently reported that deletion of the stress-regulated nuclear protein 1 (Nupr1) protected against obesity-associated metabolic alterations due to increased beta cell mass, but complete Nupr1 ablation was not advantageous since it led to insulin resistance on a normal diet. The current study used Nupr1 haplodeficient mice to investigate whether a partial reduction in Nupr1 expression conferred beneficial effects on glucose homeostasis. Islet number, morphology and area, assessed by immunofluorescence and morphometric analyses, were not altered in Nupr1 haplodeficient mice under normal diet conditions and nor was beta cell BrdU incorporation. Glucose and insulin tolerance tests indicated that there were no significant changes in in vivo insulin secretion and glucose clearance in Nupr1 haplodeficient mice, and beta cell function in vitro was normal. However, reduced Nupr1 expression decreased visceral fat deposition and significantly increased insulin sensitivity in vivo. In contrast to wild type animals, high fat diet-fed Nupr1 haplodeficient mice were not hyperinsulinaemic or glucose intolerant, and their sustained insulin sensitivity was demonstrated by appropriate insulin-induced Akt phosphorylation, as determined by Western blotting. At the molecular level, measurements of gene expression levels and promoter activities identified Nupr1-dependent inhibition of heat shock factor-1-induced heat shock protein 70 (Hsp70) expression as a mechanism through which Nupr1 regulates insulin sensitivity. We have shown for the first time that Nupr1 plays a central role in inhibiting Hsp70 expression in tissues regulating glucose homeostasis, and reductions in Nupr1 expression could be used to protect against the metabolic defects associated with obesity-induced insulin resistance.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 5, May 2015, Pages 962-969
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 5, May 2015, Pages 962-969
نویسندگان
H.C. Barbosa-Sampaio, R. Drynda, B. Liu, A.M. Rodriguez De Ledesma, C. Malicet, J.L. Iovanna, P.M. Jones, D.S. Muller, S.J. Persaud,