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.
Luque
Raul M
RM
Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA.
Park
Seungjoon
S
Kineman
Rhonda D
RD
D000375:Aging / Q000502:physiology; D000818:Animals; D005260:Female; D054439:Ghrelin / Q000502:physiology; D013006:Growth Hormone / Q000502:physiology*; D013007:Growth Hormone-Releasing Hormone / Q000502:physiology; D006801:Humans; D007031:Hypothalamus / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D008297:Male; D009765:Obesity / Q000378:metabolism; D010902:Pituitary Gland / Q000502:physiology; D012737:Sex Factors; D013004:Somatostatin / Q000502:physiology*
D054439:Ghrelin; D013004:Somatostatin; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone