| Models |
Animal species |
Pathogenesis basis |
phenotypes |
Possible drawbacks |
| Streptozotocin in combination of fat diet [89,90] |
Mouse, rat |
Induced β cell damage |
Hyperglycemia; obesity; reduced insulin secretion |
Severe β cell damage and high mortality |
| Ob/ob (always in combination with high fat diet) [91] |
Mouse |
Leptin deficiency |
obesity; Hyperglycemia and hyperinsulinmia; Developed peripheral neuropathy |
No insulin insufficiency |
| DB/DB [92] |
Mouse |
Leptin receptor deficiency |
obesity; Hyperglycemia and hyperinsulinmia; Developed peripheral neuropathy |
β cell hyperplasia; No insulin insufficiency; reduced life span |
| Zucker (fa/fa) [93] |
Rat |
Leptin receptor deficiency |
Body weight increase; Insulin resistance |
No obvious hyperglycemia |
| KK-Ay (always in combination with high fat diet) [94] |
Mouse |
A glycoprotein gene mutation |
Obesity; hyperglycemia; Insulin resistance; islet cell hyperplasia |
|
| Goto Kakizaki (GK) [95,96] |
Rat |
Highest level of glucose challenge over many generations |
resistance and impaired secretion; renal
lesion, retina abnormality and nerve changes comparable to T2DM omplications in human |
relatively slim; no decreased β cell mass |
| NSY [97] |
Mouse |
Derived from NOD mice with spontaneously developed T2DM |
Mild insulin resistance; impaired insulin secretion |
No obesity; gender difference |
| OLETF [98] |
Rat |
Selective for glucose tolerance |
Obesity; Impaired glucose tolerance; Developed non-alcoholic fatty liver disease |
Genetic variance that may have no causal relationship to diabetes itself |
| Irs1-/- Irs3-/- [99,100] |
Mouse |
Deficiency of insulin receptor substrate 1 and 3 |
Increased body weight; Hyperglyemia; hyperinsulinimia; Insulin resistance |
No fatty liver |
