PUBLICATION
Development of a Novel Zebrafish Model for Type 2 Diabetes Mellitus
- Authors
- Zang, L., Shimada, Y., Nishimura, N.
- ID
- ZDB-PUB-170505-6
- Date
- 2017
- Source
- Scientific Reports 7: 1461 (Journal)
- Registered Authors
- Keywords
- Metabolic syndrome, Type 2 diabetes
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Blood Glucose/metabolism*
- Diabetes Mellitus, Experimental/drug therapy
- Diabetes Mellitus, Experimental/etiology
- Diabetes Mellitus, Experimental/genetics
- Diabetes Mellitus, Experimental/metabolism*
- Diabetes Mellitus, Type 2/genetics
- Diabetes Mellitus, Type 2/metabolism*
- Diabetes Mellitus, Type 2/pathology
- Diet/adverse effects
- Fasting/blood
- Gene Expression Profiling
- Gene Expression Regulation*
- Glucose Tolerance Test
- Humans
- Hyperglycemia/genetics
- Hyperglycemia/metabolism*
- Hyperglycemia/pathology
- Hyperphagia/physiopathology
- Hypoglycemic Agents/pharmacology
- Insulin/genetics
- Insulin/metabolism*
- Liver/metabolism
- Metformin/pharmacology
- Pancreas/metabolism
- Sulfonylurea Compounds/pharmacology
- Zebrafish
- PubMed
- 28469250 Full text @ Sci. Rep.
Citation
Zang, L., Shimada, Y., Nishimura, N. (2017) Development of a Novel Zebrafish Model for Type 2 Diabetes Mellitus. Scientific Reports. 7:1461.
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping