Where it comes from
- Made in
- The brainstem (periaqueductal grey), the hypothalamus, and the gastrin cells of the stomach’s antrum
- Sent out by
- Fasting lowers it in the stomach, and refeeding raises it again
- Acts on
- Hypothalamic feeding circuits
- Stress axis
- Pain circuits
- Fat cells
What it does
In medicine
- No medicine copies it or blocks it, and it is not measured in people
- Its receptors have no ligands in clinical use, so nothing can act on NPBWR1 or NPBWR2 at all 1
Beyond the body’s own use
- Nothing containing it is in trials, approved or obtainable outside the laboratory
- The feeding evidence points both ways and has not been resolved: injected into the brain of a rat it reduced food intake in one laboratory’s hands 2 and increased it in another’s, where the injection went into the paraventricular nucleus 3. Dose and site differ between the two
- What is clearer is the receptor rather than the peptide: mice lacking NPBWR1 become obese in adulthood, which says the system restrains weight without saying which of its two peptides does it 4
Sources
- Shimomura et al., Identification of neuropeptide W as the endogenous ligand for GPR7 and GPR8, Journal of Biological Chemistry 2002
- Mondal et al., A role for neuropeptide W in the regulation of feeding behaviour, Endocrinology 2003
- Levine et al., Injection of neuropeptide W into the paraventricular nucleus increases food intake, American Journal of Physiology 2005
- Ishii et al., Targeted disruption of GPR7 leads to metabolic defects and adult-onset obesity, PNAS 2003
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.