کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10305864 547044 2013 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Glucocorticoid excess and the developmental origins of disease: Two decades of testing the hypothesis - 2012 Curt Richter Award Winner
ترجمه فارسی عنوان
غلظت گلوکوکورتیکوئید و علل توسعه بیماری: دو دهه تست این فرضیه - 2012 برنده جوایز کورت ریشتر
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی علوم غدد
چکیده انگلیسی
The translational studies in support of the glucocorticoid hypothesis, and demonstrating that glucocorticoids are both mediators and targets of programming, are exciting and raise the question of whether this information can be used to identify those individuals most at risk of later life disease. In a recent study we showed that alterations in DNA methylation at genes important in regulating cortisol levels, tissue glucocorticoid action, blood pressure and fetal growth, are present in adulthood in association with both early life parameters and cardiometabolic risk factors. These preliminary data add to the limited literature in humans indicating a persisting epigenetic link between early life events and subsequent disease risk. Such findings open novel avenues for further exploration of the contribution of glucocorticoids to later life disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Psychoneuroendocrinology - Volume 38, Issue 1, January 2013, Pages 1-11
نویسندگان
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