In another study, it was concluded that the major target of the GHRP-6 in vivo (both laboratory animals and humans) is the hypothalamus. From the observation, it was concluded that the GH release induced by the central GHRP-6 injections in guinea pigs was inhibited by the central action of somatostatin. Furthermore, an inhibition by somatostatin with the activated GRF neurons, induced by GHRP-6, was observed via receptors known to be located on or near the GRF themselves. This particular experiment further indicated that GHRP-6 is effectively stimulating GH release from somatotrophs through different receptors, the mechanisms of which are not yet known (Chan et al. 1989).
Taking into account the broad spectrum of TGF-β1 physiology in the fibroblasts/myofibroblasts differentiation events , we deem that the reduction of the local scar cellularity and perichondrial matrix accumulation in those animals receiving GHRP-6 could be attributable to TGFB1 transcriptional and functional switch-off. Since the predominant microscopic aspect of the GHRP-6-treated wounds was characterized by meagre cartilage scars, slimmer perichondrium membranes, and far less active cells, we hypothesize that the peptide somehow attenuates the perichondrial activation response to the trauma and/or a possible mesenchyme-to-mesenchyme redifferentiation process, thus lessening the surge of fibroblast and myofibroblasts. In line with this notion, we had documented that GHRP6 prevented hepatic stellate cells activation by reducing CD68, α-SMA, and vimentin local expressions. All these events could be primarily presided by the GHRP-6-related reduction of TGFB1 and CTGF expression in both parenchymal and nonparenchymal cells .
It has been discovered that when GHRP-6 and insulin are administered simultaneously, GH response to GHRP-6 is increased (1). However, the consumption of carbohydrates and/or dietary fats, around the administration window of GH secretagogues significantly blunts the GH release. A recent study in normal mice showed significant differences in body composition, muscle growth, glucose metabolism, memory and cardiac function in the mice being administered the GHRP-6 (2). There are still many questions regarding this fairly new compound, scientists are hoping to gain a better clinical understanding of the peptide through further research over the next few years.