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Diabetes is a common metabolic disease affecting multiple organ systems, which is often accompanied by multiple complications. The complications of diabetes involve acute or chronic lesions of the whole body, and the lesions may involve one organ, multiple organs, and multiple systems. Diabetes is expected to affect more than 400 million people worldwide by 2030 and is classified as a metabolic dysfunction associated with the homeostasis of systemic glucose levels. Therefore, suitable animal models of diabetes are urgently needed to better understand the development of metabolic dysfunction.
The morphogenesis and basic cellular structure of the zebrafish pancreas is similar to that of the mammalian pancreas, with exocrine and endocrine compartments. The endocrine compartment is composed of glucagon-secreting alpha cells, insulin-producing beta cells, somatostatin-producing delta cells, ghrelin-producing epsilon cells, and pancreatic polypeptide-producing PP cells. The cells were arranged in a manner similar to mouse islets. The signaling pathways and mechanisms of endocrine pancreas development in zebrafish are highly homologous to mammals. In addition to the pancreas, the development and function of other organ systems involved in glucose homeostasis, including the brain, liver, adipose tissue, and skeletal muscle, are conserved. The preservation of pancreatic structure and glucose homeostasis allows zebrafish to be used to identify novel targets in pancreatic-related diseases such as diabetes.
Schematic representation of zebrafifish pancreas development.
| Treatment | Zebrafish Age | Characteristics |
|---|---|---|
| Intraperitoneal injection of streptozotocin | Adult | Hyperglycemia and diabetic complications |
| Alloxane exposure through incubation or IP injection | Larvae, adult | β-cell necrosis, decreased neuromast number |
| Incubation in glucose solution | Adult | Hyperglycaemia, impaired response to inuslin, diabetic retinopathy |
| Overfeeding zebrafish with a commercial food | Adult | Hyperglycaemia, glucose intolerance, insulin resistance |
| Genetic manipulation | Zebrafish Age | Characteristics |
|---|---|---|
| Nitroreductase (NTR) expressing transgenic lines exposed to metronidazole (MTZ) through incubation or IP injection | Larvae, adult | Destroyed islet tissue, increased blood glucose levels |
| Tg(1.2ins:htBidTE−ON; LR) Induced by doxycycline and tebufenozide | Larvae | β-cell ablation, increased free glucose levels |
| Genetic manipulation | Zebrafish Age | Characteristics |
|---|---|---|
| Transgenic expression of a dominant-negative IGF-I receptor (IGF-IR) in skeletal muscle | Adult | Increased fasting blood glucose level |
| Liver specific knockdown of the insulin receptor a and b | Larvae | Hyperglycemia, insulin resistance |
| Transgenic expression of C43G human proinsulin | Larvae, adult | Normal glucose homeostasis, no loss in β-cell mass |
| Genetic manipulation | Zebrafish Age | Characteristics |
|---|---|---|
| Mutation in hnf1ba | Larvae | MODY5-like pancreas hypoplasia, reduced β-cell numbers |
| Mutation in neurod1 | Larvae | Failed endocrine cell differentiation, increased free glucose levels |
| Mutation in pdx1 | Larvae, adult | Reduced β-cell numbers, disrupted glucose homeostasis, sensitivity to overnutrition |
Creative Biogene establishes zebrafish models to study obesity, pancreatic regeneration, hyperglycemia and complications of diabetes, offering particular advantages for the study of metabolic diseases. Our zebrafish model can advance your understanding of diabetes mechanisms and provide new targets for diabetes treatment. Contact us today to discuss your goals and how we can achieve them.
References
For research use only. Not intended for any clinical use.
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