Observations of patients with type 2 diabetes using innovative research techniques – based on magnetic resonance spectroscopy, revealed that insulin resistance is the result of reduced stimulated skeletal muscle glycogen synthesis. This is due to decreased insulin-stimulated glucose transport activity (Glut 4). This disorder is probably caused by the blockage of the insulin receptor by intracellular lipids. The published hypothesis says that insulin resistance is the result of the accumulation of intracellular metabolites in skeletal muscle and hepatocytes (liver cells), which is confirmed by a number of clinical studies.

In patients suffering from type 2 diabetes who lost excessive body weight by introducing appropriate eating habits, an increase in the insulin sensitivity of liver cells was observed. In addition, a decrease in intrahepatic fat was also observed in these patients. Based on literature reports, it can be concluded that increased content of visceral adipose tissue (inside the organs) increases insulin resistance.

Understanding the cellular mechanism(s) of insulin resistance offers the prospect of better targeted and more effective therapeutic interventions for the treatment and prevention of type 2 diabetes.

Source: Petersen K.F., Shulman G.I. Etiology of Insulin Resistance, The American Journal of Medicine, Volume 119, Issue 5, Supplement 1, 2006, Pages S10-S16, ISSN 0002-9343,

https://doi.org/10.1016/j.amjmed.2006.01.009.