Abstract
In this review we described the interactions between ghrelin and the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis in children and adults with growth hormone deficiency (GHD). A possible involvement of these interactions in the pathogenesis of unexplained cases of GHD was suggested. Current research provides more and more details to the knowledge on the circadian rhythm of ghrelin. We gathered reports on the decreasing effect of Helicobacter pylori-related chronic gastritis on the number of ghrelin immunopositive cells and the consequent decrease in ghrelin serum concentration. The gastrointestinal tract microflora modification of the ghrelin action, by the mechanism of molecular mimicry, was also stressed. Moreover, the mutual relationships between ghrelin and the TSH-FT4/FT3 axis in growth and metabolic processes are described. It is to be recalled that FT4 and FT3 exert a permissive impact on IGF-1 action and, in turn, GH, in reaction mediated by IGF-1, enhances the monodeiodination of FT4 to FT3. Finally, we discussed the latest attempts to use the GH secretagogue receptor (GHS-R) analogues for possible diagnostic and therapeutic purposes.
Highlights
The problem of growth hormone (GH) deficiency (GHD), both in children and adults, is an interesting, and at the same time complicated and not fully understood phenomenon
It is known that deficiencies in the GH-insulin-like growth factor 1 (IGF-1) axis are a continuum from severe growth hormone deficiency (GHD) to complete GH insensitivity [11], for which more than 90 different mutations of the GH receptor are described [12,13], certainly there are many non-genetically determined factors significantly affecting the regulatory mechanisms of the axis in question, and at least some of them seem to be modifiable
In addition to the hypothalamic factors, such as the GHRH and GHIH, the GH-IGF-1 axis is influenced by ghrelin
Summary
The problem of growth hormone (GH) deficiency (GHD), both in children and adults, is an interesting, and at the same time complicated and not fully understood phenomenon. The latest reports suggest the possibility of abandoning tests in patients with a deficiency of at least three (3) other hormones of the anterior pituitary gland and with morphologic lesions in the pituitary area (e.g., with PSIS or after neurosurgical procedures, due to, e.g., craniopharyngioma), as well as with confirmed mutations of the genes mentioned above [1,44,45,46] In these cases, a decreased IGF-1 level at least one month after the end of rhGH therapy is considered to be a sufficient confirmation of severe GHD [44]. The reason for undertaking this research was the fact that the authors of most studies concerning GHD patients compare morning ghrelin concentration with peak GH secretion during GH stimulation tests and the results of these analyses are divergent [66,67].
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