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Transcription factor AP-2beta inhibits glucose-induced insulin secretion in cultured insulin-secreting cell-line.

Abstract：

AIM:We previously identified the transcription factor activating enhancer-binding protein-2beta (AP-2beta) gene as a new candidate for conferring susceptibility to type 2 diabetes. To ascertain the possible involvement of AP-2beta in the pathogenesis of type 2 diabetes we examined the effects of AP-2beta on glucose-induced insulin secretion. METHODS:We measured the insulin secretion stimulated by glucose, tolbutamide, or KCl in the HIT-T15 cells infected with adenovirus vectors encoding AP-2beta or LacZ (control). RESULTS:We identified clear expression of AP-2beta in isolated rat pancreatic islets and in HIT-T15 cells. Glucose-induced increase in insulin secretion was significantly inhibited in AP-2beta-overexpressing cells (LacZ, 5.0+/-0.8 ng h(-1)mg(-1) protein; AP-2beta, 1.7+/-0.2 ng h(-1)mg(-1) protein; P=0.0015), whereas insulin expression was the same in both types of cells. Tolbutamide-induced insulin secretion was also suppressed in the AP-2beta-overexpressing cells, but KCl-induced insulin secretion was not affected by AP-2beta overexpression. In addition, Kir6.2 and glucokinase expression was significantly decreased in the AP-2beta-overexpressing cells. CONCLUSION:We identified for the first time that AP-2beta expressed and functioned in insulin-secreting cell-line HIT-T15. These results suggest that AP-2beta contributes to susceptibility to type 2 diabetes by inhibiting glucose-induced insulin secretion in pancreatic beta cells.

journal_name

Diabetes Res Clin Pract

journal_title

Diabetes research and clinical practice

authors

Tsukada S,Kobayashi MA,Omori S,Unoki H,Maeda S

doi

10.1016/j.diabres.2009.06.018

subject

Has Abstract

pub_date

2009-09-01 00:00:00

pages

279-85

issue

3

eissn

0168-8227

issn

1872-8227

pii

S0168-8227(09)00260-5

journal_volume

85

pub_type

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