Format

Send to

Choose Destination
Sci Rep. 2017 May 3;7(1):1461. doi: 10.1038/s41598-017-01432-w.

Development of a Novel Zebrafish Model for Type 2 Diabetes Mellitus.

Author information

1
Graduate School of Regional Innovation Studies, Mie University, Tsu, Mie, Japan. liqing@doc.medic.mie-u.ac.jp.
2
Department of Integrative Pharmacology, Mie University Graduate School of Medicine, Tsu, Mie, Japan.
3
Department of Bioinformatics, Mie University Life Science Research Center, Tsu, Mie, Japan.
4
Graduate School of Regional Innovation Studies, Mie University, Tsu, Mie, Japan.

Abstract

Obesity is a major cause of type 2 diabetes mellitus (T2DM) in mammals. We have previously established a zebrafish model of diet-induced obesity (DIO zebrafish) by overfeeding Artemia. Here we created DIO zebrafish using a different method to induce T2DM. Zebrafish were overfed a commercially available fish food using an automated feeding system. We monitored the fasting blood glucose levels in the normal-fed group (one feed/day) and overfed group (six feeds/day) over an 8-week period. The fasting blood glucose level was significantly increased in DIO zebrafish compared with that of normal-fed zebrafish. Intraperitoneal and oral glucose tolerance tests showed impaired glucose tolerance by overfeeding. Insulin production, which was determined indirectly by measuring the EGFP signal strength in overfed Tg(-1.0ins:EGFP) sc1 zebrafish, was increased in DIO zebrafish. The anti-diabetic drugs metformin and glimepiride ameliorated hyperglycaemia in the overfed group, suggesting that this zebrafish can be used as a model of human T2DM. Finally, we conducted RNA deep sequencing and found that the gene expression profiling of liver-pancreas revealed pathways common to human T2DM. In summary, we developed a zebrafish model of T2DM that shows promise as a platform for mechanistic and therapeutic studies of diet-induced glucose intolerance and insulin resistance.

PMID:
28469250
PMCID:
PMC5431185
DOI:
10.1038/s41598-017-01432-w
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center