trustmebro.to/r/…
✓ checked
trust me, bro:
here is the receipt.
the claim

Cholecystokinin is a gastrointestinal peptide that stimulates the release of pancreatic enzymes and acts as a trophic hormone for the pancreas.

the verdict
SUPPORTED
the evidence backs this
Recorded sources
3 sources for · 0 against

Counts group repeated records of the same source within each side. They do not measure evidence strength or source independence.

Is it true that Cholecystokinin is a gastrointestinal peptide that stimulates the release of pancreatic enzymes and acts as a trophic hormone for the pancreas?

Yes. Cholecystokinin functions as a key gastrointestinal peptide that not only triggers pancreatic enzyme secretion but also acts as an important trophic factor promoting pancreatic cell growth and proliferation.

Verdict: SUPPORTED · 3 sources for, 0 against · Last checked

The analysis

The retrieved scientific literature consistently supports the claim that cholecystokinin (CCK) stimulates pancreatic enzyme release and exerts trophic (growth-promoting) effects on the pancreas, as demonstrated by in vitro and in vivo studies on acinar cell growth and receptor-mediated proliferation.

Evidence for · 3
Stimulation of pancreatic acinar cell growth by CCK, epidermal growth factor, and insulin in vitro
1986
Demonstrates that cholecystokinin (CCK) directly stimulates DNA synthesis and growth in pancreatic acinar cells in vitro.
Get citation
Logsdon, C. D. (1986). Stimulation of pancreatic acinar cell growth by CCK, epidermal growth factor, and insulin in vitro. doi.org. https://doi.org/10.1152/ajpgi.1986.251.4.g487

See more details
More for · 2
Pancreas growth, tyrosine kinase, PtdIns 3-kinase, and PLD involve high-affinity CCK-receptor occupation
1994
Establishes CCK and its analogues as potent trophic factors that promote pancreas growth via high-affinity receptor occupation.
Get citation
Rivard, N., Rydzewska, G., Lods, J. S., Martinez, J., & Morisset, J. (1994). Pancreas growth, tyrosine kinase, PtdIns 3-kinase, and PLD involve high-affinity CCK-receptor occupation. doi.org. https://doi.org/10.1152/ajpgi.1994.266.1.g62

LRG1 inhibition promotes acute pancreatitis recovery by inducing cholecystokinin Type 1 receptor expression via Akt.
2025
Identifies the cholecystokinin type 1 receptor as a crucial trophic receptor regulating acinar cell proliferation and pancreatic recovery.
Get citation
ST, L., X, Z., S, L., W, Z., Y, T., N, M., SM, S., ML, L., R, R., KF, W., C, R., RA, L., L, L., & X, W. (2025). LRG1 inhibition promotes acute pancreatitis recovery by inducing cholecystokinin Type 1 receptor expression via Akt.. doi.org. https://doi.org/10.7150/thno.110116

What does the evidence say?

The retrieved scientific literature consistently supports the claim that cholecystokinin (CCK) stimulates pancreatic enzyme release and exerts trophic (growth-promoting) effects on the pancreas, as demonstrated by in vitro and in vivo studies on acinar cell growth and receptor-mediated proliferation.

Receipt History
Anyone with this link can read the claim and its public receipt, including any personal information in that text. Open permanent receipt.
Check your own claim
Challenge the receipt
Requests are recorded for review. This does not start an automatic check or guarantee a response time.

See the evidence timeline

Citation formatting by citeproc-js (Frank Bennett) and the Citation Style Language project. Source and licenses.

This receipt is an automated verdict against our published method · not an opinion about any author or publication.
Terms · Privacy · How verdicts work