Where it comes from
- Made in
- Neurons of the brainstem (nucleus of the solitary tract) and the dorsomedial hypothalamus
- Sent out by
- Feeding, stress and the daily rhythm
- Acts on
- Hypothalamic feeding and stress circuits
- Brainstem cardiovascular centres
- Pituitary lactotrophs, in cell culture
What it does
- Reduces food intake and body weight when given into the brain
- Raises blood pressure and heart rate through the brainstem
- Releases prolactin from pituitary cells in a dish, which named it, but not clearly in the living animal
In medicine
- None; there is no PrRP medicine and no clinical assay for it
- Mice without its receptor, GPR10, become obese on an ordinary diet, which is the firmest reason to think the system matters for body weight 2
Beyond the body’s own use
- No human trial of PrRP or any analogue has been run; the whole case rests on rodents 1
- Fatty-acid-modified analogues, built so that an injection under the skin reaches the brain, reduced food intake and body weight in obese rats and mice and improved their glucose handling 3
- The name is the problem rather than the claim: PrRP released prolactin from pituitary cells in a dish, which is how it was found, but it does not clearly do so in a living animal, and satiety and stress look like its real work 1
Sources
- Hinuma et al., A prolactin-releasing peptide in the brain, Nature 1998
- Gu et al., The prolactin-releasing peptide receptor (GPR10) regulates body weight homeostasis in mice, Journal of Molecular Neuroscience 2004
- Maletínská et al., Lipidized analogs of prolactin-releasing peptide exert anti-obesity effects after peripheral administration, International Journal of Obesity 2015
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.