Initial in vitro studies suggested an absolute specificity of GHRP for GH secretion, compared to its effects on the release of other pituitary hormones. In particular the studies by Bowers, and later by the Merck group, showed that the GHRPs do not release adrenocorticotrophic hormone (ACTH) in vitro. However, in vivo, it is clear that the GHRPs do affect the release of other hormones, especially ACTH and prolactin. However in terms of in vivo activity it is clear that the GHRPs do release ACTH and prolactin in the rat, and ACTH and prolactin release in humans. Very few studies have addressed specifically the effect of GHRP on prolactin and ACTH secretion, despite the effects in vivo of GHRPs on ACTH release being comparable in magnitude to the effect of corticotrophin releasing factor in rats and in humans.
There is as yet no clear evidence that a GHRP has been produced that has full GH-releasing activity yet lacks ACTH-releasing activity, or conversely, one which only possesses ACTH-releasing activity. The possibilities inherent in a small molecule with specific ACTH releasing activity should not be ignored. We tested the potential problems caused by GHRP stimulating the hypothalamicpituitary- adrenal (HPA) axis in an animal model of obesity and Type II diabetes, the Zucker Diabetic Fatty (ZDF) rat. The obesity and diabetes of the ZDF rat is known to be sensitive to adrenal hormones and therefore in these animals we thought that the diabetogenic effects of GHRPs should be revealed. In ZDF rats we found that a GHRP analogue and hGH both stimulated body weight gain. We expected that hGH would worsen the diabetic state, which it did. The dramatic diabetogenic effect of GHRP was a surprise. Most of the responses to GHRP in this experiment could be explained by it causing GH release, but the increases in blood lipids and body fat, which were not seen with hGH, probably reflect an activation of the HPA axis by the GHRP. In rodents it is well known that the diabetogenic effects of GH are ampUfied in the presence of glucocorticoids and that all known GHRPs after acute administration raise glucocorticoid levels.
The activation of the HPA axis in combination with a stimulation of GH probably explains the dramatic diabetogenic effects of GHRP in ZDF rats. This study suggests that GHRP analogs with glucocorticoid-releasing activity should be given with caution to obese or diabetes-prone individuals. In fact elderly normal human subjects given an orally active GHRP for 4 weeks have shown increased fasting blood glucose levels. Impairments in glucose control without a reduction in body fat have also been reported in obese subjects after 8 weeks treatment with this orally active GHRP, and are similar to that seen in ZDF rats, and are probably caused by the GHRP causing both GH and adrenal steroid release. As seen in the glucocorticoid sensitive ZDF rats, even a small but consistent rise in adrenal stimulation, accompanying GH stimulation, seems to provide an undesirable extra diabetogenic drive in susceptible individuals.
The hope that GHRP administration by being more "physiological" in causing a pulsatile release of GH, would have less side effects than treatment with hGH, may not in fact be the case. Therefore structure-activity studies of GHRPs clearly need to address many issues in addition to the ability of GHRP to directly release GH from pituitary cells in vitro.
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