>Like other research groups, principally the Department of Physiology, Swedish University of Gotteborg, we took several years studying the effect of growth hormone (GH) on nerve regeneration.

We have seen his actions as a factor inducing neural stem cell proliferation and transformation of these to neurons as well as the important role the hormone plays at this level as a factor in cell survival. We have deciphered the biochemical signaling pathways involved in this process and we examined the effect neurorreparadores of the hormone in patients with acquired brain injury as well as peripheral nerve damage.

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efecto hormona crecimientoHowever, some of these effects are so immediate that continue to surprise us and leads us to think that there is something that so far eludes us. Since the Physiology and Biochemistry are pure integration of concepts, “the body functions as a whole,” today we ask a question that we leave the air for other groups of researchers to respond to it.

The effects, sometimes so immediate, the hormone can not be attributed to its role neurorregenerador. Much to form new neurons they need time to migrate, organize, integrate and begin to respond. Presumably a time longer than that often found in answers. What could be the reason for its immediacy?.

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If one recalls how is the complex control of pituitary GH secretion, as published in 1992 in Trends Endocrinol Metab, immediately displayed a series of negative feedback circuits, in which the somatostatin inhibitor tonic hormone secretion plays a key role. GH secretion, or exogenous administration, immediately lead to an increase in Somatostatin release from the hypothalamus to hypothalamic-pituitary portal circulation, in order to block the secretion of GH into the circulation. In turn, disruption of GH secretion results in a disruption of the discharge of somatostatin. Through this system, the pituitary hormone secretion occurs in a pulsatile manner, the ideal to optimize its effects at the tissue level.

But go further. The main negative regulator of somatostatin secretion is norepinephrine. This explains why a drug such as clonidine, alpha-2 adrenergic agonist, used as a stimulus to characterize the secretion of GH in the study of children with presumed deficiency of this hormone.

If we keep analyzing and integrating concepts, it seems reasonable but has not been studied, when administered GH and secondarily, as noted above, induce release of somatostatin, this leads to a rapid increase in cerebral biosynthesis of Noradrenaline. This is an important neurotransmitter of an activator, which in itself could justify the speed of certain key responses observed after treatment with the hormone, impossible to justify by a mechanism of neurogenesis. What’s more, Noradrenaline is formed from dopamine, as it increased immediately and metabolism, would lead to an increase in the bioavailability of dopamine biosynthesis and, more importantly as a neurotransmitter. That is, for the uninitiated in the subject, administration of GH would activate very important central neurotransmitter pathways, triggering thus a number of neuronal connections that might justify those answers so fast that we talked about.

If your approach is correct, something that is worth investigating, all justify the use of the hormone in degenerative processes such as Parkinson’s or Alzheimer’s, to name just two examples. Is not we who are going to do, at least for now, and we have no time to divert the current research to other fields, but from here we want to leave this door open for anyone interested in the subject can try and find out. I hope that the approach is correct, as thousands of patients and their families would benefit from it. .

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