Peptide directoryBrain, hypothalamus & pituitary

CART peptides

Satiety peptides named for the drugs that switch their gene on.

Where it comes from

Made in
The arcuate nucleus (in the POMC neurons of rodents, but not in human alpha-MSH neurons), nucleus accumbens, brainstem, pituitary, islets and gut
Sent out by
Leptin raises it; cocaine and amphetamine raise its transcript; fasting lowers it
Acts on
  • Hypothalamic feeding circuits
  • Reward circuits
  • Islets
  • Spinal cord

What it does

  • Suppresses feeding when given into the brain and curbs the reward of cocaine, though mice lacking it take cocaine as readily as others 1
  • A mutation (Leu34Phe) found in one family tracks with severe obesity across three generations 2
  • Promotes insulin release and beta cell survival

In medicine

  • No medicine copies it or blocks it. Blood CART is a research marker with no agreed assay behind it
  • Its receptor is the obstacle: GPR160 was put forward in 2021 and a later study found that CART peptide does not activate it, so the peptide is still an orphan 3

Beyond the body’s own use

  • Studied for addiction and for obesity in animals. No CART peptide has been given to a person, and there is no human medicine 1
  • Nothing containing CART is approved or obtainable outside the laboratory
  • The strongest human evidence is genetic rather than pharmacological: a mutation in the CART gene tracks with severe obesity and a lower resting energy expenditure across a large family 2

Sources

  1. Kristensen et al., Hypothalamic CART is a new anorectic peptide regulated by leptin, Nature 1998
  2. del Giudice et al., Mutational screening of the CART gene in obese children, Diabetes 2001
  3. Freitas-Lima et al., GPR160 is not a receptor of the anorexigenic CART peptide, European Journal of Pharmacology 2023

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.