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
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.