While searching, I came across this article which seems to state that Rapamycin may slow down the development of diabetes.
During the progression to T2DM there is a chronic activation of mTORC1 signaling pathway, which induces aging and acts as an endogenous inhibitor of autophagy.
I think mitochondrial effiency is one of the big paths which affects gene expression. Not surprising really. What I assume happens it that the cell presses the accelerator for more ATP, but the ATP just does not come in sufficient quantities to translate the mRNA into protein even if there is enough acetyl-CoA (and ATP) to transcribe the more complex genes in any event.
There are other aspects such as DNA damage, but I think they are less commonly a problem.
Yes, but autophagy follows a U shaped curve, so we need to be careful to not try to overdo it with multiple autophagy inducing supplements on top of rapamycin.