详细记录  
题名:Inhibitory effect of zinc on glucose-stimulated zinc/insulin secretion in an insulin-secreting beta-cell line.
作者:SLEPCHENKO KG; JAMES CB; LI YV;
来源:Exp Physiol. 2013 Aug;98(8):1301-11. doi: 10.1113/expphysiol.2013.072348. Epub [ IF= 0.00 ] ]
URL :10.1113/expphysiol.2013.072348
日期:20130902
摘要:Diminished or inappropriate secretion of insulin is associated with type II
diabetes. The cellular/molecular mechanism coupled with the regulation of insulin
secretion is still under intense investigation. Divalent ion zinc (Zn(2+)) is
co-packaged and co-secreted with insulin and is intimately involved in the
process of insulin biosynthesis and the maturation of insulin secretory granules.
The study reported here investigated glucose-stimulated zinc secretion (GSZS) and
the effect of zinc on glucose-stimulated insulin secretion (GSIS) in the HIT-T15
pancreatic beta-cell line. Zinc secretion was measured using a newly developed
fluorescent zinc imaging approach, and the insulin secretion was measured using
an enzyme-linked immunosorbent assay. There was apparent granular-like zinc
staining in beta-cells. The application of glucose induced detectable zinc
secretion or GSZS. Like GSIS, GSZS was dependent on the glucose concentration
(5-20 mm) and the presence of extracellular calcium. The application of a zinc
chelator enhanced GSZS. When brief paired-pulse glucose stimulations, which
involve the initial glucose stimulation followed by a second round of glucose
stimulation, were applied, zinc secretion or GSZS that followed the first pulse
was inhibited. This inhibition was reversed by zinc chelation, suggesting a
feedback mechanism on GSZS by zinc secreted from beta-cells. Finally, the
application of zinc (50 mum) strongly inhibited GSIS as measured by enzyme-linked
immunosorbent assay. The present study suggests that insulin secretion is
regulated by co-secreted zinc that may act as an autocrine inhibitory modulator.

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