Somatostatin-28

Where it comes from

Made in

D cells of the gut above all; some in the hypothalamus

Sent out by

Nutrients, especially fat and protein, in the small intestine

Acts on

• Pancreatic islets
• Pituitary
• Gut

What it does

• The somatostatin that actually rises in blood after a meal; somatostatin-14 barely moves ²
• More potent than somatostatin-14 at suppressing insulin, and its preference for SSTR5, the receptor the beta cell carries, is why ³
• Longer-lived in blood, so it is the form that can act at a distance rather than only on its neighbours

In medicine

• Covered by the same analogues: no approved medicine distinguishes the two forms, and pasireotide was designed for breadth across the receptors rather than for either one ³
• Measured in research only. Telling it from somatostatin-14 needs a form-specific assay, which is why most published “somatostatin” levels are a mixture

Beyond the body’s own use

• Not studied as a treatment in its own right. Its claim to attention is physiological: when antibodies were used to neutralise it alone in baboons, insulin release after a meal rose, which makes it a genuine after-meal brake rather than a processing by-product ¹
• What is not known is whether the same holds in people. Nobody has blocked somatostatin-28 selectively in a person, so its share of the normal control of insulin is an inference from one primate study ¹