“I’ve always understood that the job of insulin was to move glucose from the blood into the cell, which is why in the absence of sufficient insulin, glucose ends up hanging out in the blood, picking fights and causing trouble. So what do the inside-the-cell reactions you describe have to do with diabetic complications?” This question, posed in the comment to my post about sorbitol (the best question of the semester so far), deserves a full answer so let’s see if I can give it. First of all, you will have had to read...

Whether type 1 or type 2, the number one obsession for the diabetic individual is blood glucose. There is good reason for this. The host of complications that await the unfortunates who do not control their blood glucose level is daunting. However, glucose, advanced glycosylated endproducts (AGE), and the activation of the AGE receptor (RAGE) is only part of the problem. The other part is contributed by sorbitol. As it happens the two are tightly linked. High glucose leads to high sorbitol. If we want to understand mechanistically...

Glucose, that innocuous sweet molecule, is reactive. Chemically, what happens is that glucose has a slight reducing capacity (i.e. the capacity to accept electrons) and it is quite happy to accept electrons from the epsilon amino group of the amino acid, lysine. Lysine is found in virtually every protein and when that electron is shared it creates an irreversible chemical bond between the glucose and the protein. The protein has become glycosylated and your diabetes complications have begun. Clinically, glycosylation is a very useful...