Glossary
Somatostatin
Somatostatin acts as the brake on the growth hormone axis via five SSTR subtypes. Its two forms, its 3-minute half-life and why it matters in research design.
Somatostatin — also known as somatotropin release-inhibiting factor, SRIF — is the inhibitory opposite of GHRH within the growth hormone axis. Two bioactive forms are cut from one shared precursor, somatostatin-14 and the N-terminally longer somatostatin-28, and each contains a disulfide bridge that holds the active loop in shape.
Sources and receptors
It is made in the periventricular nucleus of the hypothalamus, in the delta-cells of the pancreatic islets and along the whole gastrointestinal tract. Somatostatin signals via five class A GPCRs, SSTR1 to SSTR5, which couple to Gi and inhibit adenylate cyclase. The reported effects are largely inhibitory: reduced release of growth hormone and TSH from the pituitary, lower insulin and glucagon secretion, and decreased exocrine output in the gut. The native peptide has a plasma half-life of about three minutes, which led to octreotide and lanreotide being developed as protease-resistant cyclic analogs for clinical use.
Its impact on secretagogue studies
Somatostatin tone acts as the feedback brake that limits secretagogue research. How much growth hormone a GHRP or GHRH analog releases depends on the point in the somatostatin rhythm at which the stimulus arrives — a frequent cause of discrepancies between studies.
Related terms
IGF-1. See the somatostatin research family and the pituitary and hypothalamus hub.