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Sci Rep. 2015 Sep 18;5:14241. doi: 10.1038/srep14241.

Diabetic pdx1-mutant zebrafish show conserved responses to nutrient overload and anti-glycemic treatment.

Author information

1
Institute of Molecular Biology/CMBI; Leopold-Francis University of Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.

Abstract

Diabetes mellitus is characterized by disrupted glucose homeostasis due to loss or dysfunction of insulin-producing beta cells. In this work, we characterize pancreatic islet development and function in zebrafish mutant for pdx1, a gene which in humans is linked to genetic forms of diabetes and is associated with increased susceptibility to Type 2 diabetes. Pdx1 mutant zebrafish have the key diabetic features of reduced beta cells, decreased insulin and elevated glucose. The hyperglycemia responds to pharmacologic anti-diabetic treatment and, as often seen in mammalian diabetes models, beta cells of pdx1 mutants show sensitivity to nutrient overload. This unique genetic model of diabetes provides a new tool for elucidating the mechanisms behind hyperglycemic pathologies and will allow the testing of novel therapeutic interventions in a model organism that is amenable to high-throughput approaches.

PMID:
26384018
PMCID:
PMC4585597
DOI:
10.1038/srep14241
[Indexed for MEDLINE]
Free PMC Article

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