Role of endogenous somatostatin in regulating GH output under basal conditions and in response to metabolic extremes.

Somatostatin (SST) was first described over 30 years ago as a hypothalamic neuropeptide which inhibits GH release. Since that time a large body of literature has accumulated describing how endogenous SST mediates its effects on GH-axis function under normal conditions and in response to metabolic extremes. This review serves to summarize the key findings in this field with a focus on recent progress, much of which has been made possible by the availability of genetically engineered mouse models and SST receptor-specific agonists.