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Regolazione Della Secrezione Dell’ormone Somatotropo: Tentativo Di Interpretazione Unitaria

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Riassunto

Gli AA. prendono in esame i varî aspetti della secrezione somatotropinica: su essa influiscono i substrati energetici, quali glucosio, NEFA e proteine (regolazione di tipo metabolico), e meccanismi di tipo catecolaminico (stress, vasopressina, pirogeni, L-dopa); è presente inoltre una secrezione ritmica di GH, la quale si verifica, con meccanismo ancora non caratterizzato, in rapporto al sonno (SWS). Mentre la stimolazione di tipo metabolico può essere inibita con la contemporanea somministrazione di glucosio, ciò non avviene per la stimolazione di tipo catecolaminico e per quella legata al sonno. Sulla base di queste premesse e del presupposto che la regolazione della secrezione di GH avviene a livello diencefalico, gli AA. avanzano un’ipotesi di interpretazione unitaria del meccanismo di controllo della secrezione somatotropinica. Il segnale metabolico e quello catecolaminico verrebbero cioè percepiti in maniera indipendente, o meglio il secondo agirebbe a valle del primo, così da non poter essere influenzato, come questo, dalla iperglicemia. Viene supposta — cioè — la presenza di un chemocettore, sensible all’informazione energetica, che trasmette il segnale con meccanismo adrenergico. La ricezione, a livello della cellula GH-RF-secernente, avverrebbe mediante recettori α. Viene infine postulata una distribuzione topografica della regolazione metabolica nel diencefalo medio-posteriore (nucleo ventromediale) e di quella legata allo stress e al sonno nel diencefalo anteriore (nucleo paraventricolare).

Résumé

Les auteurs examinent les différents aspects de la sécrétion de somatotrophine: sur celle-ci se répercutent les sub-stratums energétiques, tels que glucose, NEFA et protéines (régulation de type métabolique), et les mécanismes de type catécholaminique (stress, vasoprexine, pyrogènes, L-dopa); une sécrétion rythmique de GH est aussi présente; celle-ci se produit, par un mécanisme pas encore caractérisé, en relation au sommeil (SWS). La stimulation de type métabolique peut être interdite par l’administration contemporaine de glucose, tandis que cela ne se vérifie pas pour la stimulation de type catécholaminique et pour celle liée au sommeil. Sur la base de cette introduction et partant du principe que la régulation de la sécrétion de GH se produit au niveau diencéphalique, les auteurs avancent l’hypothèse de l’interprétation unitaire du mécanisme de contrôle de la sécrétion de somatotropine. Les signaux métabolique et catécholaminique seraient donc perçus d’une manière indépendante, ou mieux encore le deuxième agirait en aval du premier, de sorte à ne pouvoir être influencé, comme celui-ci, par l’hyperglycémie. On suppose donc la présence d’un «chemocepteur», sensible à l’information enérgétique, transmettant le signal par un mécanisme adrénergique. La réception, au niveau de la cellule GH-RF-sécrétante, se produirait par des récepteurs α. On postule enfin une distribution topographique de la régulation métabolique dans le diencéphale moyen-postérieur (noyau ventromédial) et de celle liée au stress et au sommeil dans le diencéphale antérieur (noyau paraventriculaire).

Resumen

Los autores examinan diversos aspectos de la secreción somatotropínica: en ella influyen substratos energéticos, tales como la glucosa, los ácidos grasos libres y las proteínas (regulación de tipo metabólico), y otros mecanismos de tipo catecolamínico (stress, vasopresina, pirógenos, L-dopa); se halla presente también una secreción rítmica de GH, la cual se verifica, a través de un mecanismo que todavía no ha sido caracterizado, en relación con el sueño (SWS). Mientras la estimulación de tipo metabólico puede ser inhibida con el suministro simultáneo de glucosa, no acontece lo mismo con la estimulación de tipo catecolamínico y con la vinculada al sueño. Sobre la base de esas premisas y previo presupuesto de que la regulación de la secreción de GH tiene lugar a nivel del diencéfalo, los autores avanzan una hipótesis de interpretación unitaria del mecanismo de control de la secreción somatotropínica. Es decir, que la señal metabólica y la catecolamínica serían percibidas de manera independiente o, mejor aún, la segunda actuaría debajo de la primera, sin poder, por tanto, recibir influencia por parte de la hiperglicemia, tal como le sucede a la primera. O sea, que se supone la existencia de un quemioceptor sensible a la información energética que transmite la señal con mecanismo adrenérgico. La recepción a nivel de la célula GH-RF-secretora, tendría lugar por medio de receptores α. Finalmente se formula la distribución topográfica de la regulación metabólica en el diencéfalo medioposterior (núcleo ventrículomedial) y la vinculada al sttess y al sueño en el diencéfalo anterior (núcleo paraventricular).

Zusammenfassung

Die Verfasser besprechen die verschiedenen Aspekte der Somatotropinsekretion: sie wird sowhol von Energiesubstraten wie Glukose, FFA und Proteinen beeinflusst (Regulierung vom metabolischen Typus), als auch von an Katecholamine gebundenen Mechanismen (Stress, Vasopressin, Pyrogene, L-Dopa); daneben findet sich noch eine rhythmische GH-Sekretion, deren Mechanismus noch nicht geklärt ist, im Zusammenhang mit SW-Schlaf. Während die Stimulierung vom metabolischen Typus durch gleichzeitige Verabreichung von Glukose gehemmt werden kann, ist dies für die Stimulierung vom Katecholamin-Typus und für die an den Schlaf gebundene nicht möglich. Aufgrund dieser Tatsachen und in der Annahme, dass die Regulierung der GH-Sekretion im Zwischenhirn erfolgt, setzen die Verfasser eine Hypothese zur einheitlichen Interpretation des Kontrollmechanismus der Somatotropinsekretion auseinander. Es wird angenommen, dass das metabolische und das Katecholamin-Signal unabhänging von einander empfangen werden, oder besser, dass letzteres talwärts vom ersterem wirkt, weshalb es auch, im Gegensatz zu diesem, nicht durch Hyperglykämie beeinflusst werden kann. Mit anderen Worten, es wird ein Chemozeptor angenommen, welcher für Informationen über Energiesubstrate empfindlich ist und das Signal durch einen adrenergenen Mechanismus überträgt. Der Empfang des Signals in der GH-RF-sezernierenden Zelle soll durch alpha-Rezeptoren erfolgen. Schliesslich wird folgende topographische Verteilung der Regulationszentren gefordert: die metabolische Regulation im mittleren-hinteren Zwischenhirn (Nucleus ventromedialis), die an Stress und Schlaf gebundene im vorderen Zwischenhirn (Nucleus paraventricularis).

Summary

The various aspects of growth hormone secretion are considered: it is subject to the influence of the energy substrates, such as glucose, NEFA and proteins (metabolic regulation) and to catecholamine mechanisms (stress, vasopressin, pyrogens, L-dopa); there is also a rhythmic secretion of GH, the mechanism of which is as yet undefined, related to sleep (SWS). While metabolic stimulation can be inhibited by simultaneous glucose administration, this is not so for catecholamine- or sleep-related stimulation. On the basis of these premises and of the assumption that GH secretion is regulated at the diencephalic level, a comprehensive hypothesis interpreting the control mechanism of growth hormone secretion is set out. It is suggested that the metabolic signal and the catecholamine signal are picked up independently, or rather that the second acts at a lower level than the first, so that contrary to the first it cannot be influenced by hyperglycemia. In other words the existence of a chemoreceptor is postulated which would be sensitive to information concerning energy substrates and would transmit the signal by an adrenergic mechanism. Reception in the GH-RF-secreting cell would be by α-receptors. As to topographical distribution, it is suggested that metabolic control occurs in the middle-posterior diencephalon (ventromedial nucleus) and the stress-and sleep-related control in the anterior diencephalon (paraventricular nucleus).

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Vigneri, R., Squatrito, S., Motta, L. et al. Regolazione Della Secrezione Dell’ormone Somatotropo: Tentativo Di Interpretazione Unitaria. Acta diabet. lat 10, 91–106 (1973). https://doi.org/10.1007/BF02590653

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