This is an interesting idea, but please be cautious - even in long-standing type 2 diabetes it is very unlikely to see the metabolic picture of diabetic ketoacidosis characteristic of (untreated) type 1 DM, suggesting that it is rare to reach the level of insulin (and c-peptide?) deficiency encountered in type 1 DM.

The basic difference between type I and type II diabetes mellitus lies in the nature of molecular defect. Type I DM is characterized by deficient or lack of insulin secretion by pancreatic beta cells probably due to defect in K+ channel while type II DM is characterized by insulin resistance in peripheral tissues such as skeletal muscle and adipose tissues in particular. There are differences in certain immunological and biochemical variables between the two types of diabetes. The insulin levels either remain normal or a bit elevated in Type II DM in the initial stages. However, gradual build up of insulin resistence in type II diabetics leads to gradual decrease in rate of insulin secretion. Thus, in due course of time, type II diabetics also exhibit deficient secretion of insulin as is the case with type I diabetes mellitus. However, type II diabetes is not associated with generation of autoantibodies even in later stages.

As GBKS said the fundamental difference between type1 and type 2 DM is the presence of auto antibodies in type 1 DM which is the causative factor of type 1DM .Where as type 2 DM is initially associated with insulin resistance , the reason for slight elevated levels of insulin sometimes. The dyslipedemia is more severe in Type 2 DM.Many times type 2 DM cases go unnoticed till 40% damage has occurred. In type 1DM insulin is the choice of treatment , in type 2 there is a choice of OHA

I agree with Mahendra Bhat

Diabetes is a chronic disease may have a start with Emotional (disturbances) Stress which can disturb internal homeostasis of fuel supply and utilization. Emotional Stress is associated with unwanted increase in Free Fatty Acids (alternative fuel) in blood which can lead to Insulin Resistance. This Syndrome of Insulin Resistance can be seen prior to development of Type 2 Diabetes frequently in Obese individuals as Metabolic Syndrome. Metabolic Syndrome can be detected much earlier (1-2 decades) to Type 2 DM. Through Proper Life style Changes Insulin Resistence can be corrected and development of Diabetes can be prevented. Chronic neglect of adoption of proper Life style changes leads to development of Type 2 DM (Hyperglycemia with Insulin Excess with insulin resistance) with time it can transit into Type 1 DM (Hyperglycemia with Insulin Exhaustion). Both clinical conditions can exhibit same clinical features with hyperglycemia.

I have read the above comments and agree. Basically the one feature that is similar to type 1 and late type 2 diabetes is the absence/lack of insulin secretion from the pancreas but in contrast to type 1 diabetes, insulin resistance remains a hallmark of type 2 diabetes.

i agreed but not completely.

Totally agree

Although the etiology of type 1 and type 2 diabetes differ, the complications are similar. hence one should consider what are the common factors in these 2. These are basically the hyperglycemia and the dyslipidemia, therefore they must be considered as being the principal factors involved. Whether or not insulin deficiency per se plays a part is debatable: more research needs to be done in this area

Yes, One should consider what are the common causative factors in these 2 conditions

The causative factor that is common can be subjective, ie. Emotional Stress based on subjective ignorance.

I think one difference is the time without insulin. ON DM1 is very long and all the negative effects of this are more.

Agreed

I agreed with bhatt, and add one more thing ,that meatabolic disorders like diabetis and thyroid disorders are related with emotional disorders, whether directly or indirectly,

This is a very interesting topic, which came out a few years ago under the name "accelerator hypothesis". You can read the following publication for more information about it.

Article The accelerator hypothesis: A review of the evidence for ins...

This reply is correct but in Type 2 diabetes the main longterm abnormality is insulin resistance in peripheral tissue e.g. muscles which leads to an increase in insulin secretion, until, as correctly stated, insulin secretion declines at which moment Type 1 and 2 are somewhat similar in as far insulin needs to be substituted by insulin injection.

Only when pancreatic b cell exhaustion occurs and they stop secreting insulin.

Good topic, most of the molecular and biochemical outcomes what we have understood were derived from animal studies, if u are intrested with animal models i prefer u to use db/db mice which undrgoes all stages with in short time than other models

I partly disagree as both types blend with same features. Their management might be same at this late stage in terms of insulin regimen only as T2DM might be on MFN, DPP4i or GLP-1 agonist with insulin. Co-morbidity and phenotype are mostly different.

I fully agree with Peter Bolli that insulin resistence in peripheral tissue(s) is a major difference even in late stage T2DM. In clinical practice, insulin requirements often are much higher in these T2DM patients even iif they are normal weight or at least in a weight range comparable to their T1DM counterparts. However, this should be differentiated from artificial (iatrogenic) insulin resistance that may be provoked by extremely high energy intake (high in carbohydrate) and low physical activity in T1DM patients. The phenomenen may be less common now but was seen rather often during the fifties of the 20th century when very long acting insulins where introduced and widely in use (with once daily injections), and when subsequently patients had to eat in order to avoid hypoglycemia. The clinical phenotype of these patients let them appear as "artificial T2 diabetic patients".

As a matter of facts the type of diabetic complications in type 1 diabetes may start early where marked decrease in insulin secretion is already present . This is whatever the reduction her is attributed to significant Beta cell destruction or to autoimmune influence . Later stage in type 2 is similar to certain extent where marked depletion in Insulin and C-peptide secreion is evident which mostly leads to diabetic complications . The aim of therapy in both cases is to restore the insulin in sufficient level to acheive normal metabolic pathways . Taken in consideration that Insulin resistance may be evident in type 2 however increasing insulin dose may be possible solution to the problem

Not glucose inside the cell, less Energy.

type 1 and 2 complication are simillar but not identical. a good example of this would be that majority of type 2 diabetics who lose eye sight have maculopathy as compared to type1 where many lose eye sight due to proliferative complications or advanced diabetic eye & only around 1/3 have maculopathy . another in nephropathy in type 2 where you may have nonproteinuric renal disease with pathological features of DNP while in type 1 it's soo rare to have such a disease. it would be totally agreeable to blame things on hyperglycemia but I believe that mere insulin presence in type 2 seems to be somewhat "protective" even at same level of hyperglycemia ie same HbA1c when other comparators are accounted for such as duration of hyperglycemia , dyslipidemia , blood pressure...etc which reflects that the whole pathological process which is totally different between both types play a role

Whereas type 1 diabetes is mediated by autoreacctive T lymphocytes, type 2 diabetes does not have an immune component. Some complications occur commonly in both type 1 and 2 diabetes. It has been proposed that epigenetic mechanisms may contribute to these complications as discussed in my recent editorial in Circulation Research.

For my research work, I want to induce diabetes in a new animal model: horses pony. In this species the diabetes type 2 seem to be a common disorder. How can I do to induce these pathologies, particularly for type 1, with a minimum of pain and with a risk control for the animals?

Sincerely.

Daneil G. Interesting idea. The use of Streptozotocin (IP injection) may induce Nearly type 1 DM model, but may be expensive for horses pony. Good luck!