Dear Raja,

The following publication describe the animal models used for type -2 diabetes mellitus.

http://www.ncbi.nlm.nih.gov/pubmed/9806767

FASEB J. 1998 Nov;12(14):1581-7.

Aromatic hydroxylation in animal models of diabetes mellitus.

Lubec B1, Hermon M, Hoeger H, Lubec G.

Author information

Abstract

Although the involvement of oxidative stress is well documented in the diabetic state, the individual active oxygen species generated have not been demonstrated in animal models of diabetes currently used. Since streptozotocin-induced diabetes mellitus in animals still serves as an animal model of diabetes mellitus, but streptozotocin induces diabetes and generates oxidative stress per se, we decided to study whether aromatic hydroxylation reflecting hydroxyl radical attack was found in three animal models of diabetes mellitus without streptozotocin induction or in streptozotocin-induced diabetes only. For this purpose, we compared lipid peroxidation, aromatic hydroxylation of phenylalanine, glycoxidation in genetically determined diabetic mouse strains db/db and kk, and the diabetic BB rat to these parameters in the streptozotocin-treated rat. Kidney malondialdehyde concentrations, reflecting lipid peroxidation, pentosidine, and Nepsilon-caboxymethyllysine concentrations, reflecting glycoxidation, were significantly elevated in all diabetic groups as compared to their nondiabetic mates. Aromatic hydroxylation was significantly elevated in the streptozotocin-induced diabetic state exclusively. We conclude that biochemical, pathophysiological, and treatment studies in the streptozotocin model of diabetes mellitus may be confounded by the presence of products, reactions, and tissue damage generated by aromatic hydroxylation reflecting hydroxyl radical attack. We suggest it is not the diabetic state but streptozotocin that generates the hydroxyl radical, as reflected by aromatic hydroxylation in this model.

MATERIALS AND METHODS

Animals

kk mice

Spontaneously diabetic kk mice supplied by Prof. Dr. L. Herberg (Deutsches Diabetesforschungsinstitut, Duesseldorf, Germany) were bred and kept at the Institute of Versuchstierzucht, Himberg, Austria. The kk mouse is used as a model of noninsulin-dependent DM, and the renal lesions that occur closely resemble the human diabetic nephropathy. The strain is characterized by slowly developing obesity, mild hyperglycemia, and hyperinsulinism. For the severity and progression of diabetic disease, calorie intake is all-important. Metabolic abnormalities are maximal at an age of 5 months and normalize at an age of 12 months. Hyperglycemia is mainly due to hyperinsulinism. The life span of the diabetic kk mouse is shorter than their nondiabetic siblings (ddy, nondiabetic mice with kk genetic background), which were used as control group in this study (6).

As all other experimental animals used in this study, 10 female diabetic and 10 female nondiabetic mice were kept under a day/night rhythm at 23°C and had free access to tap water and mouse cake (Altromin). Drinking volume and food intake were measured and did not differ significantly in the animal systems of noninsulin-dependent DM (kk and db/db).

Body weight for controls at the start of the experiments (8 months of age) was 21.8 ± 3.8 g, and at the end (12 months of age) was 37.2 g ± 2.4 g; for diabetic animals, body weight was 29.0 ± 4.0 g at the start and 62.5 ± 13.6 g at the end of the protocol.

db/db mice

Db/db mice and their nondiabetic siblings, the C57BL/Ks strain, were purchased from Shaw‘s farm (U.K.) and kept during the experiments at the Institut of Versuchstierzucht.

The mutation db is a unit autosomal recessive gene with full penetrance, and causes metabolic disturbances in homozygous mice resembling noninsulin-dependent DM in humans. Abnormal deposition of fat at 3–4 wk of age is followed by hyperglycemia, polyuria, and glycosuria. The diabetic condition appears to develop in two stages. In the early stage there are marked increases in the levels of plasma insulin, the rates of lipogenesis and gluconeogenesis, and low glucose oxidation; there is a reduction of β-cell granules in the islets of Langerhans, with other changes suggestive of a compensating adaptation to increased insulin demand. The late stage is characterized by a nearly normal level of circulating insulin and a marked decrease in glucose utilization, but with a continued high rate of gluconeogenesis. These findings suggest a defect in the peripheral utilization of insulin rather than in the synthesis and release of the hormone from the pancreas (7).

Ten female diabetic db/db mice and 10 matched controls were used. Their body weight at the start of the experiments (3 months of age) was 20.8 ± 3.1 g and at the end (7 months of age) was 28.2 g ± 2.7 g in the controls; for diabetic animals, body weight at the start was 43.0 ± 4.8 g and at the end of the protocol body weight was 68.5 ± 6.6 g.

BB rats

The spontaneously diabetic BB rat is an animal model of human insulin-dependent DM (8). The disease is believed to result from the selective autoimmune destruction of β-cells by cell-mediated and/or humoral responses (9 , 10). Both sexes are affected, with the incidence of DM beginning around the age of sexual maturation and reaching a peak at 80–100 days. The DM syndrome is characterized by many features of autoimmunity, including intense infiltration of islets by mononuclear cells (insulitis) and the presence of circulating antibodies against islet cells.

Ten diabetic female BB rats and 10 of their nondiabetic siblings were purchased from (Centre de Selection et dÉlevage dÁnimaux de Labaratoire C.N.R.S., Orleans, France) and housed at the Institute of Animal Breeding, Himberg, Austria. Rats with DM were treated with insulin, as recommended and described (11). The age at start of the study was 3 months; the body weight in BB with DM was 165 ± 16 g in contrast to nondiabetic BB rats, with a body weight of 153 ± 20 g.

At the end of the study period (7 months), the body weight was significantly lower in BB with DM (286±12 g, P

Dear Raja

Swiss Albino rat is the preferred  animal model for induction type -2 diabetes mellitus in rodents.

You Can also See the paper

Moulisha Biswas, Tarun Karan, Biswakanth Kar, Sanjib Bhattacharya, Suresh Kumar, Ashoke Ghosh and Pallab K. Haldar. Antidiabetic and antioxidant activity of Dregea volubilis fruit in streptozotocin-induced diabetic rat. Asian Journal of Chemistry; 23 (10): 2011. 4203-4507.

High-fat diet feeding model, leptin/leptin deficient models 

This recent paper may also be helpful. A King, J Bowe. Animal models for diabetes: Understanding the pathogenesis and finding new treatments. Biochemical Pharmacology 99 (2016) 1–10

Dear Raja,

We have...

Obese models (monogenic):

Lepob/ob mice 

Leprdb/db mice

ZDF Rats

Obese models (polygenic):

KK mice 

OLETF rat 

NZO mice 

TallyHo/Jng mice

NoncNZO10/LtJ mice

Induced obesity:

High fat feeding (mice or rats)

Desert gerbil 

Nile grass rat 

Non-obese models:

GK rat

Genetically induced models of beta cell dysfunction:

hIAPP mice

AKITA mice 

The King's paper from UK can help you. Is a review about "The use of animal models in diabetes research." (see link) http://www.ncbi.nlm.nih.gov/pubmed/22352879

My best,

L.

Article Animal models in diabetes research

Article The use of animal models in diabetes research

Book Animal Models in Diabetes Research

Article Animal models for diabetes: Understanding the pathogenesis a...

Read this article: Appropriate insulin level in selecting fortified diet-fed streptozotocin-treated rat-model of type-2-diabetes for anti-diabetic studies 

http://diabetesmeeting.conferenceseries.com/abstract/2016/appropriate-insulin-level-in-selecting-fortified-diet-fed-streptozotocin-treated-rat-model-of-type-2-diabetes-for-anti-diabetic-studies 

 In addition to what mentioned, you can look at this study:

eNOS−/− db/db mice

http://jasn.asnjournals.org/content/17/10/2664.full