Neurogastroenterology and motilitySep 20, 2014

Peptide YY, neuropeptide Y, and stress hormone influence digestion and eating during acute stress

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 28, 2026

Abstract

Upper gastrointestinal transit and fecal pellet output were significantly increased in PYY-/- mice during restraint stress.

Exogenous corticotrophin-releasing factor (CRF) increased defecation in wild type mice placed in a novel environment through CRF1 receptors.
Blocking CRF1 reduced defecation in wild type and NPY-/- mice but had no effect in PYY-/- mice.
CRF1 blockade did not impact upper gastrointestinal transit in wild type mice or food intake in PYY-/- or NPY-/- mice, but it significantly increased food intake in wild type mice.
Endogenous neuropeptide Y (NPY) may inhibit the colonic motor response induced by CRF1 activation, while Peptide YY (PYY) plays a distinct role.

Simplified

BACKGROUND: Peripheral neuropeptide Y (NPY) provides protection against the endocrine, feeding and gastrointestinal (GI) responses to stress; however, it is not yet established how it interacts with corticotrophin-releasing factor (CRF) to mediate these effects. Peptide YY (PYY) also has significant roles in GI motility and food intake but little is known about its role in stress responses.

METHODS: Upper GI transit, fecal pellet output (FPO) and feeding responses, and the role of CRF1 receptors, during restraint or a novel environment stress, were ascertained in PYY-/-, NPY-/- and wild type (WT) mice, with CRF and the CRF1 antagonist, antalarmin, injected intraperitoneally.

KEY RESULTS: Upper GI transit and FPO were significantly increased in PYY-/- mice during restraint stress. Exogenous CRF increased defecation during placement in a novel environment in WT mice through CRF1 , while CRF1 blockade reduced defecation in WT and NPY-/- mice but had no effect in PYY-/- mice. In addition, CRF1 blockade had no effect on upper GI transit in WT mice, or on food intake in PYY-/- or NPY-/- mice, but it significantly increased food intake in WT mice.

CONCLUSIONS & INFERENCES: Endogenous NPY appears to inhibit the colonic motor response induced by CRF1 activation, unlike PYY, while both peptides are required for CRF1 modulation of feeding behavior during stress. Overall, these results provide new insights into the mechanism by which PYY and NPY affect stress responses.

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Peptide YY, neuropeptide Y, and stress hormone influence digestion and eating during acute stress

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