- Relationship to Diabetes
- Type 2
Wish they did tell me that when I was diagnosed they told me nothing that's really interesting so thanks.T2D starts off as IR. The classical manifestation is: fat around the liver => decrease in the liver's insulin sensitivity => disruption to the gluconeogenesis regulatory mechanism => the liver keeps churning out glucose made from amino acids, lipids etc (note: *not* from carbs), particularly overnight and when fasting. That's the big reason for having a fasting BG as part of the standard T2D blood test panel: a high fasting BG indicates that gluconeogenesis isn't under control. Metformin's main effect comes from improving the liver's insulin sensitivity => better gluconeogensis regulation => lower fasting BG, lower "baseline" BG.
All that is just standard medicine, but it never gets explained properly at diagnosis, as far as I can see. Note that carbs have very little to do with it, whereas losing visceral fat from the liver is key. Again, this has been well understood for ever, and it's the reason why weight reduction is a key piece of T2D advice.
As T2D progresses, the pancreas starts clapping out & insulin production decreases. Full-blown T2D isn't just insulin resistance; it's also poor insulin response. Roy Taylor's big thing was to show that visceral fat is to blame for this, also, and that clearing fat from the pancreas can restore beta cell function and insulin production in T2D. So losing weight => restored gluconeogenesis regulation + restored insulin response => T2D reversed, in many cases.