详细记录  
题名:Glucose-induced inhibition of insulin secretion.
作者:HELLMAN B; GRAPENGIESSER E;
来源:Acta Physiol (Oxf). 2013 Dec 20. doi: 10.1111/apha.12217. [ IF= 0.00 ] ]
URL :10.1111/apha.12217
日期:20140102
摘要:Increase of glucose is known to elevate the concentration of cytoplasmic Ca2+
([Ca2+ ]i ) in pancreatic beta-cells and stimulate insulin secretion. However,
rise of glucose can also lower [Ca2+ ]i and inhibit insulin release. In the
present review we examine the mechanisms for this inhibition and highlight its
importance for the healthy beta-cell and the development of diabetes. It is
possible to distinguish between 30-90 sec of prompt inhibition and the late
inhibition seen after the first-phase peak of insulin release. The introductory
inhibition is characteristic of the healthy beta-cell and mediated by
sequestration of [Ca2+ ]i in the endoplasmic reticulum. This inhibition is easily
seen in studies of isolated islets but too brief to be detected in a conventional
intravenous glucose tolerance test. Coupled to simultaneous rise of glucagon the
introductory suppression of insulin release is the starting point for the
antiphase relation between the subsequent insulin and glucagon pulses. Another
effect of the initial suppression is to increase the pool of readily releasable
granules responsible for the first-phase release of insulin. The presence of late
inhibition of insulin release is an indicator of beta-cell dysfunction. Patients
with type-2 diabetes often respond to intravenous bolus injection of glucose with
5-10 min of late suppression of circulating insulin. This article is protected by
copyright. All rights reserved.

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