کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10752682 | 1050329 | 2015 | 4 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inwardly rectifying Kir2.1 currents in human β-cells control electrical activity: Characterisation and mathematical modelling
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کلمات کلیدی
AMPKAction potential firingPIP2I–V - I - VInsulin secretion - ترشح انسولینPancreatic beta-cells - سلول های بتای پانکراسphosphatidylinositol 4,5-bisphosphate - فسفاتیدیلینوزیتول 4،5-بیسفسفاتElectrical activity - فعالیت برقMathematical model - مدل ریاضیaction potential - پتانسیل عمل Membrane potential - پتانسیل غشاء 5′ adenosine monophosphate-activated protein kinase - پروتئین کیناز فعال شده با آدنوزین مونوفسفات 5 'Ion channels - کانال های یونی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Pancreatic β-cells fire action potentials as do cardiac cells and neurons, and electrical activity plays a central role in glucose-stimulated insulin secretion, which is disturbed in diabetes. The inwardly rectifying Kir2.1 potassium channels (KCNJ2 gene) control cardiac electrical activity by stabilising the interspike interval. Loss-of-function abnormalities in cardiac Kir2.1 currents can lead to the long QT syndrome and alterations of cardiac excitability, and patients with some forms of long QT syndrome suffer from over-secretion of insulin, hyperinsulinemia and symptomatic hypoglycemia. The KCNJ2 gene is also expressed in human pancreatic islets, and we show that functional Kir2.1 currents are present in human β-cells. We characterised the human Kir2.1 β-cell current, and included it in a recent mathematical model of electrical activity in human β-cells. Based on our simulations we propose that Kir2.1 currents control the interspike interval, and predict that blocking Kir2.1 channels increases the action potential frequency, which should augment the rate of insulin secretion. Vice versa, the model suggests that hyperactive Kir2.1 channels may lead to reduced insulin secretion. Our findings provide a putative link between increased insulin secretion and the long QT syndrome, and give novel insight into normal and disturbed β-cell function.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 459, Issue 2, 3 April 2015, Pages 284-287
Journal: Biochemical and Biophysical Research Communications - Volume 459, Issue 2, 3 April 2015, Pages 284-287
نویسندگان
Michela Riz, Matthias Braun, Xichen Wu, Morten Gram Pedersen,