کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1991434 | 1541009 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dihydrotestosterone deteriorates cardiac insulin signaling and glucose transport in the rat model of polycystic ovary syndrome
ترجمه فارسی عنوان
دی هیدروتستوسترون باعث انتقال سیگنالینگ و انتقال گلوکز قلب در مدل موش سندرم تخمدان پلی کیستیک می شود
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کلمات کلیدی
LDMDHTNEFAPCOSGLUTBCAIRSERK1/2 - ERK1 / 2MAPK - MAPKAkt - آکتHomeostasis model assessment - ارزیابی مدل HomostasisNonesterified fatty acids - اسیدهای چرب غنی شدهinsulin receptor substrate - انسولین بستر گیرندهbicinchoninic acid - بیسینکنینیک اسیدTriglycerides - تریگلیسریدGlucose transporter - حمل و نقل گلوکزglucose transporters - حمل و نقل گلوکزDihydrotestosterone - دی هیدروتستوسترونPolycystic ovary syndrome - سندرم تخمدان پلی کیستیکPlasma membrane - غشای پلاسماHeart - قلب Insulin signaling pathway - مسیر سیگنالینگ انسولینHOMA - هومprotein kinase B - پروتئین کیناز Bmitogen-activated protein kinase - پروتئین کیناز فعال با mitogeninsulin receptor - گیرنده انسولین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
It is supposed that women with polycystic ovary syndrome (PCOS) are prone to develop cardiovascular disease as a consequence of multiple risk factors that are mostly related to the state of insulin resistance and consequent hyperinsulinemia. In the present study, we evaluated insulin signaling and glucose transporters (GLUT) in cardiac cells of dihydrotestosterone (DHT) treated female rats as an animal model of PCOS. Expression of proteins involved in cardiac insulin signaling pathways and glucose transporters, as well as their phosphorylation or intracellular localization were studied by Western blot analysis in DHT-treated and control rats. Treatment with DHT resulted in increased body mass, absolute mass of the heart, elevated plasma insulin concentration, dyslipidemia and insulin resistance. At the molecular level, DHT treatment did not change protein expression of cardiac insulin receptor and insulin receptor substrate 1, while phosphorylation of the substrate at serine 307 was increased. Unexpectedly, although expression of downstream Akt kinase and its phosphorylation at threonine 308 were not altered, phosphorylation of Akt at serine 473 was increased in the heart of DHT-treated rats. In contrast, expression and phosphorylation of extracellular signal regulated kinases 1/2 were decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased, as well as the expression of GLUT4 in cardiac cells at the end of androgen treatment. The obtained results provide evidence for alterations in expression and especially in functional characteristics of insulin signaling molecules and glucose transporters in the heart of DHT-treated rats with PCOS, indicating impaired cardiac insulin action.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 141, May 2014, Pages 71-76
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 141, May 2014, Pages 71-76
نویسندگان
Snežana TepavÄeviÄ, Danijela VojnoviÄ MilutinoviÄ, Djuro Macut, Zorica Žakula, Marina NikoliÄ, Ivana BožiÄ-AntiÄ, Snježana RomiÄ, Jelica BjekiÄ-Macut, Gordana MatiÄ, Goran KoriÄanac,