Understanding Type 2 Diabetes
Progress on the mechanisms of age-related diabetes is noted at the PENN Medicine newsroom: "When a type 2 diabetic eats a meal, insulin cannot stop the manufacture of glucose in the liver, but it can stop the burning of fat stores. This gives the diabetic person a 'double whammy:' fatty acids accumulate from food and from the liver. Consequently, more fat is deposited in tissues and obesity worsens. Until now there was no clear connection between insulin and the control of fat metabolism. This study shows that when insulin is present, as it is after a meal, the protein Akt2/PKB adds a phosphate group to its molecular partner PGC-1a. When this happens, PGC-1a cannot activate the genes needed for fat metabolism. ... if a drug could induce Akt2/PKB to add the phosphate group (phosphorylation) to PGC-1a, then the liver of a diabetic might be 'fooled' into stopping the oxidation of fat stores." This sort of "finger in the growing crack in the dam" approach to medicine is inefficient in comparison to methods of prevention - type 2 diabetes is very avoidable, after all. Relying on the medicine of the future to rescue you from conditions you could have prevented or minimized doesn't strike me as a good strategy - the medicine of the future already has a mountain to climb in the defeat of unavoidable age-related degeneration.
Link: http://www.uphs.upenn.edu/news/News_Releases/jun07/diabetes-protein-target.html