详细记录  
题名:Glucose-induced inhibition of insulin secretion.
作者:HELLMAN B; GRAPENGIESSER E;
来源:Acta Physiol (Oxf). 2014 Mar;210(3):479-88. doi: 10.1111/apha.12217. Epub 2014 [ IF= 0.00 ] ]
URL :10.1111/apha.12217
日期:20140408
摘要:Increase in glucose is known to elevate the concentration of cytoplasmic Ca(2+)
([Ca(2+) ]i ) in pancreatic beta-cells and stimulate insulin secretion. However,
rise of glucose can also lower [Ca(2+) ]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 60 and 90 s 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 [Ca(2+) ]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.

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