Abstract:
:Expression of the multi-PDZ protein Pdzd2 (PDZ domain-containing protein 2) is enriched in pancreatic islet beta cells, but not in exocrine or alpha cells, suggesting a role for Pdzd2 in the regulation of pancreatic beta-cell function. To explore the in vivo function of Pdzd2, Pdzd2-deficient mice were generated. Homozygous Pdzd2 mutant mice were viable and their gross morphology appeared normal. Interestingly, Pdzd2-deficient mice showed enhanced glucose tolerance in intraperitoneal glucose tolerance tests and their plasma insulin levels indicated increased basal insulin secretion after fasting. Moreover, insulin release from mutant pancreatic islets was found to be twofold higher than from normal islets. To verify the functional defect in vitro, Pdzd2 was depleted in INS-1E cells using two siRNA duplexes. Pdzd2-depleted INS-1E cells also displayed increased insulin secretion at low concentrations of glucose. Our results provide the first evidence that Pdzd2 is required for normal regulation of basal insulin secretion.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Tsang SW,Shao D,Cheah KS,Okuse K,Leung PS,Yao KMdoi
10.1016/j.mce.2009.11.007subject
Has Abstractpub_date
2010-02-05 00:00:00pages
263-70issue
1-2eissn
0303-7207issn
1872-8057pii
S0303-7207(09)00572-3journal_volume
315pub_type
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