Hormonal
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.
Your body uses specific gut hormones (CCK, GLP-1, PYY) to tell your brain when to stop eating. These are released in response to nutrients, especially fats and proteins, in the intestine. While these signals are crucial for normal eating, simply relying on stomach stretching (volume) is less effective than consuming nutrient-dense foods that trigger these hormonal pathways.
Satiation results from a coordinated series of neural and humoral signals that emanate from the gut in response to mechanical and chemical properties of ingested food.
Why this rating
The paper is a comprehensive review citing numerous animal and human studies, including genetic knockout models and clinical trials.
Source
Gastrointestinal regulation of food intake
David E. Cummings et al. · Journal of Clinical Investigation · 2007
DOI 10.1172/jci30227
More from this paper
- 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
- 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.Good
- 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
Related findings · Hormonal
- Initial treatment for type 2 diabetes should be a combination of metformin and either an SGLT-2 inhibitor or a GLP-1 receptor agonist to achieve cardiorenal protection, rather than monotherapy or older agents like sulfonylureas.Strong
- For patients with specific monogenic obesity syndromes (leptin deficiency, POMC/PCSK1/LEPR mutations), targeted pharmacotherapy (recombinant leptin or setmelanotide) is highly effective and should be prioritized, unlike in polygenic obesity.Strong
- Continued weekly administration of 2.4 mg subcutaneous semaglutide prevents weight regain and promotes further weight loss in adults with overweight or obesity, whereas switching to placebo results in significant weight regain.Strong
This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →