Unknown

Dataset Information

0

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


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.

SUBMITTER: Kimmel RA 

PROVIDER: S-EPMC4585597 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

altmetric image

Publications

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

Kimmel Robin A RA   Dobler Stefan S   Schmitner Nicole N   Walsen Tanja T   Freudenblum Julia J   Meyer Dirk D  

Scientific reports 20150918


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 respon  ...[more]

Similar Datasets

| S-EPMC6604603 | biostudies-literature
| S-EPMC9279356 | biostudies-literature
| S-EPMC5513979 | biostudies-literature
| S-EPMC8016283 | biostudies-literature
| S-EPMC384792 | biostudies-literature
| S-EPMC2409314 | biostudies-literature
| S-EPMC3215967 | biostudies-literature
| S-EPMC2920847 | biostudies-literature
| S-EPMC10216501 | biostudies-literature
| S-EPMC2785695 | biostudies-literature