genuine question about incretin that I am slightly embarrassed to ask
Been lurking in c/researchpeptides for about 13 months and finally have something worth posting.
Short version: week 48, 5mg, and gastric emptying is the bit I still cannot get a straight answer on. I have read the wiki, I have read the last 13 threads, and the answers split roughly down the middle.
What I actually want to know is whether the people saying it does not matter have measured it, or whether it is just repeated confidently. Happy to be told I am overthinking this — I probably am — but I would rather overthink it now than at week 42.
best — the order this archive was captured in
Flair changed to match the content. Read the sidebar before posting next time and we are square.
This is correct. Rodent data is investigational, not predictive.
This is correct.
Yes, exactly this, and it is the bit that took me 48 weeks to accept.
glucagon-receptor contribution is pharmacology for dual and triple agonism
Not convinced. The evidence does not support that reading.
receptor distribution matters, GLP-1 is not everywhere
Where does the incretin data actually come from?
the 17-day half-life means week 17 is still ramp-up pharmacokinetically
rodent incretin tells you what to investigate, not what to expect in humans
Strongly agree. Central appetite is real but people overstate it.
receptor distribution matters, GLP-1 is not everywhere
Strongly agree.
Adding to this: half-life is doing more work than the comment implies.
the 24-day half-life means week 24 is still ramp-up pharmacokinetically
mechanistic speculation is welcome if flaired as speculation
Where does the incretin data actually come from?
Edit to your parent would help — the concentration you quoted assumes one scenario and you have written another above it.
cite the paper: journal, year, first author, links optional
Stomach physiology changed when I moved up to 12.5mg. Gastric emptying lag is the whole story.
gastric emptying is real and explains most early injection-site soreness
do not extrapolate rodent data to human dosing without saying so
Yeah, the incretin mechanism is doing the work here.
Which paper are you quoting?
the half-life is appetite, affects steady state timing
do not extrapolate rodent data to human dosing without saying so
The confident tone is doing a lot of work that the evidence is not.
Rodent, human, or in vitro?
central appetite signalling is real but people overweight it
- 1Flair changed to match the content. Read the sidebar before posting next…18 comments in this branch · started by u/gastric_emptying_g
- 2Yeah, the incretin mechanism is doing the work here.7 comments in this branch · started by u/ingrid_correia