Review Article
ASV Prasad
Abstract
The fully developed syndrome of type 2 diabetes mellitus (DM2), as known to everyone, is characterised by fasting hyperglycaemia and post pranidal hyperglycaemia together. Of the two, fasting hyperglycaemia occurring earlier than postprandal hyperglycaemia is also well recognised. It implies that full blown picture of DM2 develops in successive steps. Like-wise there might be some more stages by which DM 2 passes before it is fully established, though they may not be recognised, because of late presentation of patients in the course of development of DM2. This article intends to focus on such an intermediary stage, where the FBS is already high but the post pranidal blood sugar (PPBS) is still in euglycaemic stage. The early events in the pathogenesis of DM2 are reviewed as to which out of these factors is responsible for the syndrome under consideration. The relative pros and cons of the earlier suggestions are examined to arrive at the conclusion that, the glucose transporter 2 (GLUT 2) inhibitions is probably the cause of this syndrome. The one explanation could explain fasting hyperglycaemia and GLUT 2 inhibition is traced to increased FFFs (Free Fatty Acids) / induction of B oxidation of fats in DM2.