Research
Hormonal
Propionate metabolism in the liver stimulates hepatic gluconeogenesis, which activates hepatic vagal afferents to signal satiety to the brainstem, a mechanism well-established in ruminants but less defined in humans.
Propionate from fiber fermentation may contribute to satiety via liver signaling, but this is likely a secondary effect compared to direct gut hormone release in humans.
LimitedQualifiesLOW confidence
Data obtained from animal models suggest that elevating hepatic energy status can modulate appetite and feeding behaviour through the stimulation of hepatic vagal afferents that signal to the nucleus of the solitary tract within the brainstem.
Why this rating
Strong evidence in ruminants; emerging but less definitive evidence in humans.
Source
Control of appetite and energy intake by SCFA: what are the potential underlying mechanisms?
Edward S. Chambers et al. · Proceedings of The Nutrition Society · 2014
DOI 10.1017/s0029665114001657
narrative_reviewCited 338×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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- Elevated colonic production of short-chain fatty acids (SCFA) via fermentable dietary fiber intake suppresses appetite and energy intake by stimulating the release of anorectic hormones PYY and GLP-1 through FFAR2 receptor activation on colonic L-cells.Moderate
- Acetate, a primary SCFA, crosses the blood-brain barrier to directly stimulate the hypothalamic arcuate nucleus, increasing POMC (anorexigenic) and decreasing AgRP (orexigenic) neuron expression.Moderate
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