Some people say that if you do it neonatally, it creates pattern reminding DM2.

There is no perfect animal model for disease in humans, but adjusting the dose of streptozotocin is achieved to reduce the circulating insulin, which is useful to study aspect hypoglycemic. However, if your goal is to study resistance to the action of insulin, which is a characteristic of type 2 diabetes, do not recommend it.

STZ specifically destroys beta cells, and in adult mice can also result in a pancreatic inflammatory response, although this is not the same as the autoimmunity of type 1 diabetes. It really is not a model of either type 1 or type 2 diabetes but a mechanism to reduce beta cell number creating a hyperglycemic state. This is useful for studies of beta cell plasticity, but is not a good model for human disease.

Depending on the strain of rats, STZ induces type 1 diabetes and low dosages of 35mg.kg.bw prior to feeding a high fat diet can induce type 2 diabetes.

The STZ model has been criticized for a long time. I agree with David J Hill for this point. Anyway, if you need a protocol of establishment of a rat model of T2DM from STZ , you can find details in my paper published in Molecular and Cellular Endocrinology 307 (2009) 89–98. Full text can be found in my profile

STZ will cause beta cell destruction only, whereas in type 2 diabetes it is insulin resistance which is the major etiology, for which STZ model is of no use.  

Since STZ disrupts pancreatic beta cells, it can be used for research in diabetes. Disruption of pancreatic beta cells by STZ depends on animals model and dose of STZ. In rats, single higher dose of STZ i.e. >60 mg/kg, i.p. develops type 1 diabetes mellitus. Whereas, in mice multiple dose of 35 mg/kg, i.p., STZ  and in rats single dose of 40-55 mg/kg, i.p., STZ develop type 2 diabetes mellitus. 

We cannot say it will produce type2 diabetes .  It may produce lesser beta cell damage .It cannot be called as amodel for Type2DM.

Hi!, streptozotocin (STZ) is the most commonly used agent to induces type 1 DM (Ozkol et al. J. Membrane Biol. 2013;246(1):47–55. and Rakieten et al, Cancer Chemother. Rep. 1963; 29:91–98). Also STZ-induced DM displays the characteristics of hyperglycaemia, insulin deficiency, and chronic pro-inflammatory state (Belotto et al Clin. Exp. Immunol. 2010;162:237–243).

The streptozotocin is a drug that causes toxicity in beta cells of the pancreas. However, there is sufficient scientific evidence to show that depending on the administered dose can be simulated in animal models of type 1 diabetes or type 2 diabetes with respect to the amount of insulin the pancreas produce the animal receiving the corresponding dose .

Depending on the dose applied then, could destroy all beta cells, so that the animal does not produce insulin (type 1 diabetes) or destroy only some causing the animal to produce less insulin, producing a moderate hyperglycemia, weight gain in the Animal and most likely insulin resistance caused by metabolic imbalance.  We affirm this, based on various publications, which could send you, and as a result of the experience in this direction in our laboratory.

In our laboratory we use  Intraperitoneal injection of STZ in Sprague Dowley male young adults  circa 180 g of weight  at a dose of 65mg causing Type I Diabetes.  Type II diabetes  may be obtained with  35 mg of STZ Intraperitoneal injection  after a high fat diet . The authors claim that this model show insulin resistance, hyperglycemia and the other biomarkers of Type II diabetes and suggest that this model may be useful for therapeutic aproach.

streptozotocin (STZ) is a common agent used to induce diabetes. it causes beta cell destruction. the type of diabetes depends on the dose of STZ .higher dose (more than 60 mg/kg) developes type I. while type II is induced by relative low dose of STZ comined with high fat diet.

High fat diet with lesser dose of STZ may mimick T2 DM. As there is no typical model for T2DM . This can be considered as amodel now. 

As a definition, STZ cause a pancreatic damage, then insulin secretion fall, this type of Diabetes is like the Human type I, but when STZ is applied to rats at low doses by intravenous or intraperitoneal treatment on the day of birth has been recognized as a NIDDM (Type 2) inductor, with mild hyperglycemia, impaired response to the glucose tolerance test, and a loss of B cell sensitivity to glucose.

I recommend you this free review

Szkudelski T. The mechanism of alloxan and streptozotocin action in B cells of the rat pancreas. Physiol Res. 2001;50(6):537-46. Review. PubMed PMID: 11829314.

Intraperitoneal injection of STZ will demage the beta cell, this is similar to type I diabetes. But it also be used to produce type II diabetes. My opinion is that this is not appropriate. The reason is type II diabetes mainly due to insulin resistance.

Streptozotocin enters the B cell via a glucose transporter (GLUT2) and causes alkylation of DNA. DNA damage induces activation of poly ADP-ribosylation, a process that is more important for the diabetogenicity of streptozotocin than DNA damage itself. Poly ADP-ribosylation leads to depletion of cellular NAD+ and ATP. Enhanced ATP dephosphorylation after streptozotocin treatment supplies a substrate for xanthine oxidase resulting in the formation of superoxide radicals. Consequently, hydrogen peroxide and hydroxyl radicals are also generated. Furthermore, streptozotocin liberates toxic amounts of nitric oxide that inhibits aconitase activity and participates in DNA damage. As a result of the streptozotocin action, B cells undergo the destruction by necrosis.

Now what is the question of less damage to Beta cell and more damage to beta cell? . Once it is toxic and causes necrosis to beta cell. We cannot quantify and say T2DM. 

Multiple low doses (40 mg/kg what we used in our monkey model)  of STZ induces beta cell destruction (I can not say it's autoimmune really, but insulin dependent) whether given IP or IV. 

injection of STZ  result in destruction of beta cell and induction for type one diabetes in

At lower repeated doses Type 2 diabetes phenotype can be produced. Using large dose, one can create Type-1 phenotype.

My Heartful thanks to all that i know about the induction of diabetes by your valuable answers.  But i want to know after the induction of diabetes using STZ in albino rat models how do we identify and confirm it whether it induced type I or Type II diabetes.

Once again I Thank you all.

Since doseor doses of STZ only affect total mass of beta cells and thereby phenotype, you can only indirectly assess that. STZ induced near total destruction of beta cells is not same as one sees in Type 1 diabetes mellitus arising de novo which has autoimmune basis and therefore accompanied by presence of autoantibodies directed at islets or beta cell specific antigens. 

In these models via STZ you can induce insulin dependency, which was the result of loss of beta cell mass. I believe you need to show T infiltration in the pancreatic tissue. In working with monkey STZ model for years, I preferred using multiple low doses (which also give you total beta cell loss over a period of time) of STZ to induce the more auto immune like phenomenon with T cell infiltration. Selection of animals based on MHC class II (DQB) seemed crucial in this. Large doses in my model were counter productive. Having said that, I do not wish to extrapolate those observations to rodents.

Since streptozotocin causes death of the beta cell, then depending on the applied dose was varying causes cell death which involves more or less plasma insulin concentration. Also some authors state that can be obtained hyperglycemia and moderately elevated for several months by injecting high doses of streptozotocin to neonatal rat. This can have a good application in the study of hypoglycemic than in the study of diabetes.

Dear Elavarasi,

I would say that STZ does neither exactly. If you kill all beta cells, you will have a model of insulin dependent diabetes of sorts, but without the immune effects that are hallmark of type 1 diabetes.

Even worse to try to model type 2 diabetes using STZ. None of the metabolic considerations will be part of your model. You need to ask yourself what question am I trying to answer? Only then can you know if there is any use for STZ in your study. It can be useful to kill beta cells prior to islet transplantation studies, for example. Some try to do partial depletion of beta cells as a model of T2D, but I question how useful that aproach is, it really depends on the study design, for example, asking if a pharmacological agent can improve glycemia in the face of decreased insulin secretion might be possible, but there are reports of beta cell regeneration after STZ treatment so again, one must be cautious.

Be very careful what question you are asking. I don't think that the question "does STZ cause T1 or 2 diabetes" is relevant without having an idea of how you intend to use the model.

Good luck!

http://genomemedicine.com/content/4/4/35