Research
Hormonal
Pharmacological administration of cholecystokinin (CCK) reduces meal size acutely in humans and animals, but chronic administration fails to produce sustained weight loss due to compensatory increases in meal frequency.
While CCK reduces meal size when given, the body compensates by eating more often, so it doesn't help with long-term weight loss. This highlights why simply trying to 'stop eating' with one-off interventions often fails.
GoodQualifiesHIGH confidence
Chronic CCK administration in animals, with up to 20 peripheral injections per day, reduces meal size, but this is offset by increased meal frequency, leaving body weight unaffected.
Why this rating
Supported by multiple animal and human studies, though clinical trials for obesity failed.
Source
Gastrointestinal regulation of food intake
David E. Cummings et al. · Journal of Clinical Investigation · 2007
DOI 10.1172/jci30227
narrative_reviewCited 1,196×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Gastrointestinal satiation signals, specifically cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), regulate meal termination and size through neural and hormonal pathways to the hindbrain, acting synergistically with gastric distention.Strong
- Glucagon-like peptide-1 (GLP-1) receptor agonists, such as exenatide, promote progressive weight loss in humans over up to two years while improving glycemic control, distinguishing them from other diabetes treatments that often cause weight gain.Strong
- Ghrelin is the only known hormone that powerfully increases food intake, with levels surging before meals and suppressing after eating, playing a key role in meal initiation and hunger.Good
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