Increased basal insulin secretion in Pdzd2-deficient mice

Siu Wai TSANG, D. Shao, K. S.E. Cheah, K. Okuse, P. S. Leung, K. M. Yao*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

8 Citations (Scopus)


Expression of the multi-PDZ protein Pdzd2 (PDZ domain-containing protein 2) is enriched in pancreatic islet β cells, but not in exocrine or α cells, suggesting a role for Pdzd2 in the regulation of pancreatic β-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.

Original languageEnglish
Pages (from-to)263-270
Number of pages8
JournalMolecular and Cellular Endocrinology
Issue number1-2
Publication statusPublished - 5 Feb 2010

Scopus Subject Areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

User-Defined Keywords

  • Gene-trap mutagenesis
  • Glucose-stimulated insulin secretion
  • INS-1E
  • K channel
  • Pdzd2


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