In the next day or few, I'm going to be discussing diabetes. What it is, and what the science says causes it -- at least to the current state of knowledge and understanding. This will serve as a prelude to a larger discussion on hyperinsulinemia and insulin resistance in the pathogenesis of Type 2 diabetes. Diabetes is β-cell dysfunction. Period. This does not mean that other organs and the organism as a whole are not involved in this dysfunction developing, but diabetes is, ultimately, an insulin deficiency syndrome. If that sounds "off" because of the hyperinsulinemia associated with T2, stay tuned!
So I'm going to cobble together a few sources to introduce (or reintroduce) some terminology and basics of β-cell function that will be used in future posts on this.
Molecular Formation of Insulin
On a molecular level, the final product, insulin, starts out as preproinsulin, is converted to proinsulin and then finally to the insulin. This is shown schematically below:
