Is insulin resistance caused by isomers embedding into cell membranes?

I have a theory that insulin resistance of type2 diabetes is caused by man-made isomers (such as trans isomers of fatty acids) embedding into our cell membranes. Because they are geometric isomers, they can integrate into the structure of cell membranes YET still result in the loss of functionality of that component. For example binding of insulin to receptors may fail if the structure of that receptor is composed from a geometric isomer of one of it's components.

I'm actually a physicist with a casual interest in this area. I had this idea which seemed to make sense to me . If I am correct then could we not heal ourselves of insulin resistance simply by altering our diets so that we only eat natural foods (giving up trans fats in particular) for a period of say a year will give sufficient time for the cells in our body to have been completely replaced thus healig our body of type 2 diabetes. I have heards that such measures have proved remarkably sucesfull in reducing effects

Insulin resistance is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Insulin resistance in fat cells results in hydrolysis of stored triglycerides, which elevates free fatty acids in the blood plasma. Insulin resistance in muscle reduces glucose uptake whereas insulin resistance in liver reduces glucose storage, with both effects serving to elevate blood glucose. High plasma levels of insulin and glucose due to insulin resistance often leads to the metabolic syndrome and type 2 diabetes.

The most common type of insulin resistance is associated with obesity and metabolic syndrome. This was first described in the 1930's by H.P. (Harry) Himsworth (University College Hospital Medical School, London). He described results of experiments in an article in 1936, entitled, "Diabetes Mellitus: Its differentiation into insulin sensitive and insulin insensitive types." He found that those with diabetes can be differentiated into two types: those in whom injected insulin produces an immediate suppression of hyperglycemia; and those in whom the insulin has little or no effect. Hyperglycemia itself can lead to insulin resistance, but N-acetylcysteine and taurine can prevent this effect[1].

Insulin resistance denotes decreased sensitivity of target cells (muscle, adipose and hepatic cells) to insulin. The very common "metabolic syndrome" is the concomitant appearance of diabetes mellitus (type 2), hypertension, combined hyperlipidemia and central obesity. It is also associated with polycystic ovarian syndrome (PCOS).

In obese patients, compensatory hyperinsulinemia reduces the expression of the membrane insulin receptor (down regulation) which maintains the maximal response. More importantly, defects in processes within the cell itself (also called post-receptor defects) appear to play a much larger role in the development of insulin resistance. A relationship between leptin resistance and insulin resistance has been suggested.

In a normal person, insulin is released from the beta cells of the Islets of Langerhans located in the pancreas after eating ("postprandial"), and it signals the body to allow glucose to enter insulin-sensitive tissues (e.g., muscle, adipose) and maintain normal blood glucose levels. In an "insulin resistant" person the message does not get through to those cells until much more insulin is released in an attempt to compensate. Occasionally, this can lead to a steep drop in blood sugar and a hypoglycaemic reaction several hours after the meal.

Insulin resistance is often associated with visceral adiposity (increased waist cicumference), hypertension, hyperglycemia and dyslipidemia involving elevated triglycerides, small dense low-density lipoprotein (sdLDL) particles, and decreased HDL cholesterol.

Insulin resistance is also often associated with a hypercoagulable state (impaired fibrinolysis) and increased inflammatory cytokine levels.

It is difficult to say that insulin resistance can be caused by isomers embedded into the cell membranes (fatty acids) only since Insulin resistance is also associated in hypercoagulable states. Also, there are other possible causes of Insulin resistance such as prolonged use of medications like Rifampicin, Isoniazid, Olanzapine, Risperidone, Antiretrovirals. Lastly, genetic causes have been addressed such as the Donohue Syndrome which displays insulin receptor mutations, and LMNA mutations (Familial Partial Lipodystrophy).

Good luck on your research and let me know if you have published a study concerning Type 2 Diabetes. Report It

I have type 2 diabetes my pancreas does not produce any insulin at all, a diet alteration would ultimately kill me not cure me, it's insulin I need to break down the carbohydrates and combat an excess of sugar.
I suggest you really read into the subject of diabetes before making any other statement that a naive diabetic might think is a miracle cure and end up with such high sugar levels he dies

insulin stimulates GLUT transporters which take in glucose, and i would think the transporters are mostly protein based so i dont think this is possible, but im a pharm student not an expert so who knows. that is an interesting theory though. type 2 diabetes is basically insulin insensitivity and i dont think the receptors ever regain full effectiveness once you are a type 2. if you eat mostly healthy foods and excercise youre unlikely to get type 2 diabetes anyway unless its genetic, so the best "cure" for type 2 diabetes is just to avoid the risk factors.

the other problem is that most people who are diabetic eat junk and dont excercise enough in the first place, and people rarely change