Where it comes from
- Made in
- Hypothalamus, posterior pituitary and the adrenal
- Sent out by
- With vasopressin; fasting raises it
- Acts on
- Vasopressin neurons
- Orexin neurons of the lateral hypothalamus
- Islets (insulin, in vitro)
What it does
In medicine
- No medicine copies it or blocks it, and it is not measured in people
- It has no identified receptor. Its feeding effect is abolished by an orexin receptor blocker, so what it binds first is still unknown 2
Beyond the body’s own use
- Nothing containing it is in trials, approved or obtainable outside the laboratory
- It is the more interesting half of the pair: as well as restraining vasopressin like NERP-1, it increases food intake and movement, and that effect disappears when orexin signalling is blocked, which places it upstream of the wake-and-feed system 2
- What is unknown is how one precursor coordinates three jobs. VGF yields NERP-1, NERP-2 and TLQP-21, which act on water balance, feeding and fat, and nothing is known about what decides which of them a cell makes 3
Sources
- Yamaguchi et al., Peptidomic identification and biological validation of neuroendocrine regulatory peptide-1 and -2, Journal of Biological Chemistry 2007
- Toshinai et al., Neuroendocrine regulatory peptide-2 regulates feeding behaviour via the orexin system, American Journal of Physiology 2010
- Toshinai & Nakazato, Neuroendocrine regulatory peptide-1 and -2, bioactive peptides processed from VGF, Cellular and Molecular Life Sciences 2009
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.