Vnitr Lek 1999, 45(12):729-733

[Etiopathogenesis of type 2 diabetes mellitus].

K Kubát, M Zboril: Interna I, MN Litomĕrice.

In the genesis and development of type 2 diabetes in the great majority of subjects the contemporary lifestyle characterized by inadequate physical activity and an excessive energy intake is of basic importance. The majority of abnormalities and defects revealed by laboratory tests is probably secondary and caused by the above mentioned factors. Contemporary views of the etiopathogenesis of the disease are demotivating for patients: if the cause of their disease were an inborn disorder at the level of transmission of a signal on membranes then probably nothing else can be done than to take prescribed drugs. If the mistake involves the lifestyle, the latter can be changed and the disease avoided. Any medicamentous treatment is associated with the risk of undesirable effects--the complication of hyperinsulinism in treatment with sulphonyl urea derivatives and insulin or lactate acidosis after treatment with biguanides. This risk is not influenced by early prevention: dietary restraint and adequate physical exercise. Diabetes type 2 and 1--despite the common sign of hyperglycaemia--are characterized by a fundamental difference: (not influenced by treatment) DM type 1 is characterized by enhanced catabolic processes, starvation at the cellular level. Type 2 is characterized by enhanced anabolic processes, excessive amounts of nutrients in cells. The authors submit recommendations which respect the secondary character of deviations for the development of DM 2 which can be detected by laboratory methods: The following are the basic etiopathogenetic mechanism for the development of DM 2: 1. Chronic excessive intake and inadequate output of energy a) increased nutrient supply to the liver with secondary increase of gluconeogenesis in the liver, b) chronic increased supply of glucose to peripheral tissues, in particular muscles and adipose tissue, inadequate physical exercise, with secondary restriction of nutrient supplies to these tissues. 2. Secondary affection of insulin secretion in the islets of Langerhans in the pancreas.