hi Somaia,

To appreciate the relevance of a specific animal model for human T2D, it is important to try to mimic the pathology of the human condition as much as possible. second, what you want to study: is it insulin resistance?  obesity-related metabolic disorder? the pathophysiologic basis for drug development and therapy?

you have to have a question first.even drug screening  will differ in results from one model to another. allow me to recommend some literature. hope you will find what you are looking for.

salam.

http://ilarjournal.oxfordjournals.org/content/47/3/186.long#sec-7

http://ilarjournal.oxfordjournals.org/content/47/3/181.long

hi Somaia,

To appreciate the relevance of a specific animal model for human T2D, it is important to try to mimic the pathology of the human condition as much as possible. second, what you want to study: is it insulin resistance?  obesity-related metabolic disorder? the pathophysiologic basis for drug development and therapy?

you have to have a question first.even drug screening  will differ in results from one model to another. allow me to recommend some literature. hope you will find what you are looking for.

salam.

http://ilarjournal.oxfordjournals.org/content/47/3/186.long#sec-7

http://ilarjournal.oxfordjournals.org/content/47/3/181.long

We got a very good result by inducing the rats with Poloxamar-407, a surfactant for T2DM. You can get the papers through the link:

https://www.researchgate.net/profile/Supriya_Krishnan2/contributions

The studies assessing the physiological and biochemical effects of bioactivities of natural or synthetic products in humans are logistically and methodologically complex. Therefore we should rely on laboratory animal models of treatment and computational docking protocols that mimic the treatment response in humans. Now a day, the PX-407 induced diabetic rats are commonly used as an animal model of human T2D to study pathophysiological characteristics, in addition to therapeutic influences. PX-407 induction to neonatal rats at the dose of 10 mg/kg b.w. intraperitoneally, increases body weight, manifest hyperglycemia, an impaired response to the glucose tolerance test and loss of β-cell sensitivity to glucose. These alterations in biochemical parameters are inevitable, when the unrestrained diabetic status advances, considerable modifications in these biochemical indices are expected. Some of the published papers can be found from the given link:

https://www.researchgate.net/profile/Supriya_Krishnan2/contributions

You can either use directly ob/ob or db/db mice (leptin/leptin receptor ko) or set mice on a high fat diet and induce insulin resistance..

 streptozotocin  i.v 50mg/kg

As rightly pointed out by Thomas, you may go for commercially available ob/ob or db/db mouse or create a diabetic animal model by feeding lab mice with high fat chow; we use unto 60% fat chow for some of our studies.

Not all models are the same and no one can completely reproduce the multifactorial components that cause T2D. However you can look for some specific changes with the above mentioned models. You should take in account that you must validate in your lab that your proposed model actually develop insulin resistance and persistent hyperglycemia.  

Many experimental animal research teams have induced insulin resistance/persistent- hyperglycemia in offspring by manipulating maternal diet during pregnancy and/or lactation. A wide variety of maternal diets have been used to achieve this.  Our group has used a low protein (7 percent energy) maternal diet throughout pregnancy and lactation.  Insulin resistance and hyperglycemia has also been induced in offspring with total energy restricted diets and, as mentioned above, high fat maternal prenatal diets.  Our studies have revealed that IR and hyperglycemia induced by the low protein maternal diet can be exacerbated if the offspring are weaned to a high saturated fat diet.  IR and hyperglycemia are observed even if the animals are weaned on to control chows, however.  Our group has shown that this phenotype persists across at least two additional generations (F3) even when (F1) female offspring are weaned to control diets and maintained on control diets during their own pregnancies.

http://www.ncbi.nlm.nih.gov/pubmed/10736323

http://www.ncbi.nlm.nih.gov/pubmed/15051426

http://www.ncbi.nlm.nih.gov/pubmed/16557373

http://www.ncbi.nlm.nih.gov/pubmed/18928547

You can use streptozotocin 60 mg/kg i p.  I used this and it worked for me but make sure that after 24-48 hours of induction, you start checking the glucose level, otherwise the glucose level might be so high above 300 mg/dl and this could result into hyperglycaemia and eventual deaths of the animals(rats to be precise) before the commencement of your treatment options. Moreover, alloxan can also be used but in some cases, the animals can recover from the damage after few days of the induction. I have tested and witnessed this. I hope this information is of benefit

streptozocin can be used or 2deoxy bglucose which mimics conventional glucose -reast is as above.

Sreptozotocin has been used by many researchers to induce both T1D and T2D, depending on the concentration that is administered. Attached is a research paper that might be of help

You can use Streptozotocin, alloxan or Fructose. Another method is to induce insulin resistance (IRS) which is strictly specific for type-2 diabetes.

Why don't try by using palmitic oil ?

A combination of high fat diet for a couple of weeks followed by a single injection of low dose streptozotocin, below 40 mg/kg body weight may also give you type 2 diabetic mice models.  

Hi Somaia,

To my knowledge, commonly used laboratory animals do not develop type 2 diabetes. As you mentioned, the diabetes caused by STZ and ALX may has some attributes similar to T2DM, but etiologically these models are clearly T1D because all of them are based on destroying beta cells.

However, there is a strain of minipigs called Ossabaw that is vulnerable to metabolic syndrome and also develops T2DM after a certain period of feeding with high-fat atherogenic diet. In recent study, researchers even reached fasting plasma glucose >300 mg/dl (attached).

I think this model is only available at the Indiana University, but we're planning to establish it also in Europe. Please feel free to contact me if you are interested in this model.

Bye

Tamas

http://physiology.medicine.iu.edu/people-in-physiology/michael-sturek-ph-d/

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