This constitutive activity seems to provide a tonic signal required for the development of normal height, probably through an effect on the GH axis.

[15] It was also found that, when GHS-R1A constitutive activity was diminished, there were decreased levels of hunger-inducing hormone neuropeptide Y (NPY) as well as in food intake and body weight.

[9] It is well-characterized that activating the growth hormone secretagogue receptor with ghrelin induces an orexigenic state, or general feeling of hunger.

[18] Second, it was found that specifically activating the receptor in just the hippocampus increased both long-term potentiation (LTP) and dendritic spine density, two cellular phenomena thought to be involved in learning.

[8] Third, short-term calorie restriction, defined as a 30% reduction in caloric intake for two weeks, which naturally increases ghrelin levels and thus activates the receptor, was found to increase both performance on spatial learning tasks as well as neurogenesis in the adult hippocampus.

GHS-R agonists have appetite-stimulating and growth hormone-releasing effects, and are likely to be useful for the treatment of muscle wasting and frailty associated with old-age and degenerative diseases.

This article incorporates text from the United States National Library of Medicine, which is in the public domain.