Where it comes from

Made in
The pituitary’s intermediate lobe (vestigial in adults), hypothalamic POMC neurons, and skin
Sent out by
With alpha-MSH, to which it is the other half
Acts on
  • Pancreatic islets (insulin release, in animals)
  • Brain (sleep)

What it does

  • A fragment of it, ACTH 22-39, was isolated from obese mice as an insulin secretagogue and named beta-cell-tropin 1
  • Given into the rat brain it lengthens REM sleep, an effect that persists after the pituitary is removed 2
  • Its presence marks that POMC was cut the intermediate-lobe way, yielding alpha-MSH and CLIP rather than ACTH 3

In medicine

  • None of its own; there is no clinical assay for CLIP, and whether an ACTH antibody detects it depends on which end of the molecule that antibody recognises
  • Which cells make it is the clinical point rather than any action: CLIP marks the intermediate-lobe route of POMC processing 3

Beyond the body’s own use

  • There is no CLIP product and no human trial; everything claimed for it rests on two old animal findings
  • The insulin one is the stronger: ACTH 22-39 behaved identically to the natural beta-cell-tropin of obese mice and potentiated glucose-driven insulin release 1
  • The sleep one is thinner: ten nanograms of CLIP into the rat brain increased paradoxical sleep, and nothing comparable has been attempted in people 2
  • What is unknown is whether CLIP has a receptor at all; it does not activate the melanocortin receptors and no other has been identified for it

Sources

  1. Beloff-Chain et al., Evidence that the insulin secretagogue beta-cell-tropin is ACTH 22-39, Nature 1983
  2. Chastrette et al., POMC-derived peptides and sleep in the rat, Neuropeptides 1990
  3. Bicknell, The tissue-specific processing of pro-opiomelanocortin, Journal of Neuroendocrinology 2008

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.