someone explain incretin to me like I have not read a paper in years
someone explain incretin to me like I have not read a paper in years. Searched first, found three threads that contradict each other, hence the post. GLP-1 receptor agonism acts both peripherally — insulin secretion in a glucose-dependent way, slowed gastric emptying — and centrally, on appetite regulation. The…
The mental model, in four steps, that makes the rest of this site legible.
One: gut hormones amplify the insulin response to food. Two: agonists at those receptors act peripherally on insulin secretion and gastric emptying, and centrally on appetite. Three: structural modification gives them a long half-life, so exposure is smooth and weekly. Four: tolerance develops to some effects and not to others.
From those four, most of what the experience boards report falls out: why the side effects cluster early, why they settle at a stable dose, why appetite reduction persists, and why the scale and the appetite move on different clocks.
The half-life explanation was the thing that made weekly dosing intuitive for me rather than arbitrary.
Started reading limitations sections first. It has changed how much weight I give to almost everything posted here.
Started reading limitations sections first.
This is the concept everything else on this board is downstream of.
Push back: a receptor being expressed in a tissue does not tell you the agonist reaches it at therapeutic exposure.
Left up and flaired Explainer. This is the standard of post the board was created for.
dose response is not linear and nobody should assume it is