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Increased basal insulin secretion in Pdzd2-deficient mice
S W Tsang1, D Shao, K S E Cheah
1Department of Biochemistry, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Molecular and Cellular Endocrinology
|November 26, 2009
Summary
PDZ domain-containing protein 2 (Pdzd2) regulates insulin secretion. Pdzd2-deficient mice exhibit enhanced glucose tolerance and increased insulin release, indicating Pdzd2
Area of Science:
- Endocrinology
- Molecular Biology
- Metabolic Research
Background:
- PDZ domain-containing protein 2 (Pdzd2) expression is specific to pancreatic islet beta cells.
- This specificity suggests a regulatory role for Pdzd2 in beta-cell function.
Purpose of the Study:
- To investigate the in vivo function of Pdzd2 in the regulation of pancreatic beta-cell function and glucose homeostasis.
- To determine the necessity of Pdzd2 for normal insulin secretion.
Main Methods:
- Generation and analysis of Pdzd2-deficient mice.
- Intraperitoneal glucose tolerance tests (IPGTTs).
- Measurement of plasma insulin levels and in vitro insulin secretion assays from isolated islets and INS-1E cells with Pdzd2 depletion via siRNA.
Main Results:
- Pdzd2-deficient mice displayed enhanced glucose tolerance and increased basal insulin secretion after fasting.
- Insulin release from mutant pancreatic islets was twofold higher than from wild-type islets.
- Pdzd2-depleted INS-1E cells showed increased insulin secretion at low glucose concentrations.
Conclusions:
- Pdzd2 is essential for the normal regulation of basal insulin secretion.
- The study provides the first evidence linking Pdzd2 to the control of insulin release and glucose metabolism.
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