Pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus: the role of skeletal muscle glucose uptake and hepatic glucose production in the development of hyperglycaemia. A critical comment
- Cite this article as:
- Beck-Nielsen, H., Hother-Nielsen, O., Vaag, A. et al. Diabetologia (1994) 37: 217. doi:10.1007/s001250050097
Our understanding of the pathophysiology of Type 2 diabetes has advanced considerably over the last decade, but many problems and issues remain unresolved. The initiation of this debate mirrors many of the problems that we face today. An understanding of the primary and secondary defects leading to diabetes in “genetically prone” individuals are of crucial importance to further our understanding of the metabolic process involved in the development of the diabetic state. In our contribution to this debate we have pointed out the methodological problems that have arisen in the estimation of HGP and the quantitation of glucose kinetics in normo-and hyperglycaemic Type 2 diabetic individuals. These problems are not yet completely resolved. Therefore, the importance of the liver vs the importance of muscle glucose metabolism in the development of hyperglycaemia will probably have to wait for new and improved techniques. However, the current data strongly indicate that the primary defect (genetic defect?) in insulin action is located to skeletal muscles.
The near-normal HGP values in Type 2 diabetes patients with fasting blood glucose values less than 12–15 mmol/1 do not indicate that the insulin sensitivity of liver is normal in Type 2 diabetes, but proves to us that the reduction in insulin action in both liver and muscles are fully compensated —perhaps slightly overcompensated.