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11. Adaptation of the 24-h growth hormone profile to a state of sleep debt

Author

SPIEGEL, K., LEPROULT, R., COLECCHIA, E. F., L'HERMITE-BALERIAUX, M., NIE, Z., COPINSCHI, G., and VAN CAUTER, E.

Subjects
Somatotropin -- Physiological aspects, Secretion -- Regulation, Sleep deprivation -- Research, Slow wave sleep -- Physiological aspects, Men -- Health aspects, Biological sciences
Abstract

Adaptation of the 24-h growth hormone profile to a state of sleep debt. Am J Physiol Regulatory Integrative Comp Physiol 279: R874-R883, 2000.--In normal men, the majority of GH secretion occurs in a single large postsleep onset pulse that is suppressed during total sleep deprivation. We examined the impact of semichronic partial sleep loss, a highly prevalent condition, on the 24-h growth hormone profile. Eleven young men were studied after six nights of restricted bedtimes (0100-0500) and after 7 nights of extended bedtimes (2100-0900). Slow-wave sleep (SWS) was estimated as the duration of stages III and IV. Slow-wave activity (SWA) was calculated as electroencephalogram power density in the 0.5- to 3-Hz frequency range. During the state of sleep debt, the GH secretory pattern was biphasic, with both a presleep onset 'circadian' pulse and a postsleep onset pulse. Postsleep onset GH secretion was negatively related to presleep onset secretion and tended to be positively correlated with the amount of concomitant SWA. When sleep was restricted, both SWS and SWA were increased during early sleep. Unexpectedly, the increase in SWA affected the second, rather than the first, SWA cycle, suggesting that presleep onset GH secretion may have limited SWA in the first cycle, possibly via an inhibition of central GH-releasing hormone activity. Thus neither the GH profile nor the distribution of SWA conformed with predictions from acute sleep deprivation studies, indicating that adaptation mechanisms are operative during chronic partial sleep loss. growth hormone secretion; slow-wave activity; sleep deprivation

Published
2000

13. Eighth annual meeting of the European Association for the Study of Diabetes: Madrid, Spain September, 6–8, 1972

Author

Alberti, K. G. M. M., Darley, J., Emerson, Pauline M., Hockaday, T. D. R., Amherdt, M., Like, A. A., Blondel, B., Marliss, B., Wollheim, C., Orci, L., Andersen, O. Ortved, Andersson, Arne, Antonini, F. M., Fumagalli, C., Petruzzi, E., Bertini, G., Mori, S., Tinti, P., Ashcroft, S. J. H., Weerasinghe, L. C. C., Randle, P. J., Assan, R., Slusher, N., Guy-Grand, B., Girard, F., Soufflet, E., Attali, J. R., Ballerio, G., Boillot, J., Atkins, T., Matty, A. J., Bailey, C. J., Aynsley-Green, A., Bloom, S. R., Bacchus, R. A., Meade, L. G., London, D. R., Balant, L., Zahnd, G., Petitpierre, B., Fabre, J., Balasse, E. O., Neef, M. A., Barta, L., Brooser, G., Molnar, Maria, Bataille, D. P., Freychet, P., Kitabgi, P., Rosselin, G. E., Berne, Christian, Beyer, J., Cordes, U., Sell, G., Rosak, C., Schöffling, K., Birkner, B., Henner, J., Wagner, P., Erhardt, F., Dieterle, P., Bloom, S. R., Vaughan, N. J. A., Edwards, A. V., Boquist, L., Brand, I., Söling, H. D., Brandenburg, D., Gliemann, J., Ooms, H. A., Puls, W., Wollmer, A., Camerini-Davalos, R. A., Bloodworth, Jr., J. M. B., Limburg, B., Oppermann, W., Campbell, A. K., Siddle, K., Cañadell, J. M., Barraquer, J., Muiños, A., Heredia, C. D., Castillo-Olivares, J., Guijo, J., Pallardo, L. F., Cerasi, E., Efendić, S., Luft, R., Cerasi, E., Wahren, J., Luft, R., Felig, P., Christensen, Niels Juel, Christiansen, A. H., Vølund, A., Connon, J. J., Trimble, E., Copinschi, G., Leclercq, R., Bruno, O. D., Cordes, U., Sell, G., Beyer, J., Haupt, E., Schöffling, K., Creutzfeldt, C., Track, N. S., Cuendet, G. S., Wollheim, C. B., Cameron, D. P., Balant, L., Stauffacher, W., Marliss, E. B., Czyzyk, A., Lao, B., Bartosiewicz, W., Szczepanik, Z., De Nobel, E., Laar, A. Van't, Koene, R. A. P., Benraad, Th. J., Dietze, G., Hepp, K. D., Wickmayr, M., Mehnert, H., Dixon, K., Exon, P. D., Hughes, H. R., Jones, D. W., Elkeles, R. S., Exon, P. D., Dixon, K., FitzGerald, M. G., Malins, J. M., Falorni, A., Massi-Benedetti, F., Gallo, G., Maffei, S., Fedele, D., Tiengo, A., Muggeo, M., Fabris, P., Crepaldi, G., Federlin, K., Helmke, K., Slijepčević, M., Pfeiffer, E. F., Felber, J. P., Oulès, J., Schindler, Ch., Chabot, V., Fernandez-Cruz, Jr., A., Catalán, E., Otero, M. Luque, Hermida, O. Garcia, Otero, M. Luque, Catalán, E., Flatt, J. P., Blackburn, G., Randers, G., Förster, H., Hoos, I, Lerche, D., Förster, H., Hoos, I., Matthäus, M., Franckson, J. R. M., Ooms, H. A., Frerichs, H., Daweke, H., Gries, F., Grüneklee, D., Hessing, J., Jahnke, K., Keup, U., Miss, H., Otto, H., Puls, W., Schmidt, D., Zumfelde, C., Funcke, H. v., Löffler, G., Wieland, O., Galton, D. J., Guttman, R., Gazzola, G. C., Franchi, R., Ronchi, P., Saibene, V., Guidotti, G. G., Gligore, V., Hîncu, N., Tecuceanu, Rodica, Goberna, R., Garcia-Albertos, F., Tamarit-Rodriguez, J., del Rio, E., Roca, R., Gomez-Acebo, José, Creco, A. V., Fedeli, G., Ghirlanda, G., Fenici, R., Lucente, M., Gutman, A., Agam, G., Nahas, N., Cazalis, P., Gylfe, E., Hellman, B., Hadden, D. R., Connolly, J. H., Montgomery, D. A. D., Weaver, J. A., Hellerström, Claes, Howell, Simon, Andersson, Arne, Edwards, John, Sehlin, J., Täljedal, I. -B., Heptner, W., Neubauer, H. B., Herchuelz, A., Pipeleers, D. G., Malaisse, W. J., Herrera, E., Montoya, Eladio, Hommel, H., Fischer, IT., Schmid, B., Fiedler, H., Bibergeil, H., Iversen, J., Iynedjian, P. B., Peters, G., Jacquemin, C., Lambert, B., Sutter, B. Ch. J., Jakob, A., Zapf, J., Froesch, E. R., Jansen, F. K., Freytag, G., Herberg, L., Jarrett, R. J., Baker, I. A., Jarrousse, C., Rancon, F., Rosselin, G. E., Job, D., Tchobroutsky, G., Eschwege, E., Guyot-Argenton, C., Aubry, J. P., Déret, M., Karman, H., Mialhe, P., Kissebah, A., Tulloch, B., Fraser, Russell, Kissebah, A., Tulloch, B., Vydelingum, N., Fraser, Russell, Kissing, J., Raptis, S., Dollinger, H., Faulhaber, J., Rothenbuchner, G., Pfeiffer, E. F., Kleineke, J., Sauer, H., Söling, H. D., Kloeze, J., Kohner, Eva M., Sutcliffe, Barbara A., Tudball, M., Dollery, C. T., Korp, W., Neubert, J., Bruneder, H., Lenhardt, A., Levett, R. E., Koschinsky, T., Gries, F. A., Landgraf-Leurs, M. M. C., Landgraf, R., Hörl, R., Langslow, D. R., Laube, H., Fussgänger, R., Mayer, R., Pfeiffer, E. F., Laube, H., Fussgänger, R., Klör, H., Pfeiffer, E. F., Lázaro, E., Leclercq-Meyer, V., Marchand, J. J., Malaisse, W., Ledet, Thomas, Lefébvre, P. J., Luyckx, A. S., Le Marchand, Y., Assimacopoulos, F., Singh, A., Amherdt, M., Rouiller, Ch., Jeanrenaud, B., Lenti, G., Frezzotti, R., Angotzi, G., Bardelli, A. M., Pagano, G., Basetti-Sani, A., Galli, M., Lernmark, Å., Fex, G., Lindsay, D. G., Loge, O., Lopez-Quijada, C., Chiva, L., Rodriguez-Lopez, M., Loten, E. G., Loubatières, A. L., Loubatières-Mariani, M. M., Ribes, G., Chapal, J., Lubetzki, J., Duprey, J., Sambourg, Cl., Lefebvre, P. J., Maier, V., Hinz, M., Schatz, H., Nierle, C., Pfeiffer, E. F., Malaisse, W. J., Pipeleers, D. G., Malaisse-Lagae, F., Orci, L., Malaisse-Lagae, F., Amherdt, M., Ravazzola, M., Stauffacher, W., Orci, L., Renold, A. E., Manzano, P., Rojas-Hidalgo, E., Marco, J., Diaz-Fierros, D., Calle, C., Roman, D., Villanueva, M. L., Valverde, I., Marliss, E. B., Wollheim, C. B., Blondel, B., Orci, L., Like, A., Amherdt, M., Stauffacher, W., Massi-Benedetti, F., Luycks, A. L., Fracassini, F., Lefebvre, P. J., Falorni, A., Menzel, R., Michaelis, D., Neumann, I., Bibergeil, H., Schulz, B., Wilke, W., Wulfert, P., Krämer, K., Menzinger, G., Fallucca, F., Tamburrano, F., Carratu', R., Andreani, D., Metzger, P., Franken, P., Balasse, E. O., Michael, R., Hildmann, W., Jutzi, E., Michl, J., Fankhauser, S., Schlichtkrull, J., Mirouze, J., Orsetti, A., Vierne, Y., Arnoux, N., Mølsted-Pederson, L., Tygstrup, Inge, Villumsen, Åge L., Pedersen, Jørgen, Montague, W., Howell, S. L., Moody, A. J., Agerbak, G. S., Sundby, F., Muggeo, M., Crepaldi, G., Fedele, D., Baritussio, A., Naeser, Peter, Navalesi, R., Pilo, A., Lenzi, S., Cecchetti, P., Corsini, G., Donato, L., Nerup, J., Andersen, O. Ortved, Bendixen, G., Egeberg, J., Poulsen, J. E., Nielsen, J. Høiriis, Hansen, F. Mølgaard, Gliemann, J., Niki, A., Niki, H., Koide, T., Lin, B. J., Nikkels, R. E., Terpstra, J., Gay, A., Oakman, R. H., Lazarus, Norman R., Orci, L., Amherdt, M., Stauffacher, W., Like, A. A., Rouiller, C., Renold, A. E., Malaisse-Lagae, F., Ravazzola, M., Ostman, J., Backman, L., Cerasi, E., Luft, R., Hallberg, D., Ostrowski, K., Panten, U., Christians, J., Parving, H. -H., Rasmussen, S. Munkgaard, Marichal, M., Platilovà, H., Dufek, M., Konopàsek, E., Pozuelo, V., Tamarit, J., Suner, A., Castell, C., Pruett, E. D. R., Maehlum, S., Raptis, S., Grebe, B., Chrissiku, M., Rothenbuchner, G., Müller, R., Hinze, H. J., Pfeiffer, E. F., Reinauer, H., Müller-Ruchholtz, E. R., Rietzler, X., Passa, P., Canivet, J., Schatz, H., Otto, J., Hinz, M., Maier, V., Nierle, C., Behrens, G., Bücher, T., Pfeiffer, E. F., Schlumpf, U., Morell, B., Zingg, A., Schönborn, J., Westphal, P., Panten, U., Bloom, G. D., Idahl, L. -A., Lernmark, A., Söderberg, M., Rios, M. Serrano, Hawkins, F. G., Escobar, F., Mato, J. M., Larrodera, L., de Oya, M., Rodriguez-Miñon, J. L., Shafrir, E., Gutman, A., Sitbon, G., Mialhe, P., Skrabalo, Z., Panajatović, N., Papić, Z., Posinovec, J., Stavljenić, A., Lipovac, V., Aganović, I., Soler, N. G., Bennett, M. A., Söling, H. D., Peters, H., Janson, G., Sönksen, P. H., Srivastava, M. C., Tompkins, C. V., Nabarro, J. D. N., Sørensen, N. Schwartz, Ladefoged, K., Wildenhoff, K. E., Sorge, F., Diehl, H. -J., Hoffmann, H., Schwartzkopff, W., Standl, E., Kolb, H., Standl, A., Mehnert, H., Sutherland, H. W., Stowers, J. M., Whetham, J. C. G., Sutter, B. C. J., Billaudel, B., Sutter, B. Ch. J., Sutter-Dub, M. T., Leclercq, R., Jacquot, R., Täljedal, I. B., Tamarit, J., Tamarit-Rodriguez, J., Goberna, R., Gobema, R., Tamás, Jr., Gy., Baranyi, Éva, Baranyi, A., Radvanyi, A., Tatoń, J., Hinek, A., Wiśniewska, A., Tattersall, R. B., Pyke, D. A., Terpstra, J., Slot, J. Bruins, Sande, P. L. M. v. d., Radder, J. K., Waldeok, K. J. J., Muijden, R. C. P. A. v., Tiengo, A., Assan, R., Frerichs, H., Creutzfeldt, W., Turner, D. S., Baker, R. W., Gent, W. G. L., Shabaan, A., Marks, V., Young, D. A. B., Vague, Ph., Heim, H., Laval, C. Martin, Vegezzi, M., Campo, C.Di, Rahamandridona, G., Garron, D., Heyraud, B., Vague, J., Valverde, I., Villanueva, M. L., Lozano, I., Diaz-Fierros, M., Marco, J., Van Assche, F. A., Gepts, W., Van Obberghen, E., Somers, G., Devis, G., Vaughan, G. D., Malaisse-Lagae, F., Orci, L., Malaisse, W. J., Veleminsky, J., Spirova, E., Waldhäusl, W., Frisch, H., Haydl, H., Weiss, L., Löffler, G., Wieland, O., Willms, B., Deuticke, U., Wollheim, C. B., Marliss, E. B., Blondel, B., Orci, L., Like, A., Renold, A. E., Zrůstová, M., and Roštlapil, J.

Published
1973
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17. Editorial

Author

Copinschi, G., primary, Touraine, P., additional, and Beck-Peccoz, P., additional

Published
2007
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45. A benzodiazepine hypnotic facilitates adaptation of circadian rhythms and sleep-wake homeostasis to an eight hour delay shift simulating westward jet lag.

Author

Buxton, O M, Copinschi, G, Van Onderbergen, A, Karrison, T G, and Van Cauter, E

Abstract

To determine whether appropriately timed administration of a short-acting benzodiazepine hypnotic, which has proven effective in an animal model of jet lag, also facilitates adaptation of circadian rhythmicity and sleep-wake homeostasis in a human model of jet lag.

Published
2000

46. Le Traitement De Lintoxication Barbiturique Aicue

Author

Cornil A, Thys O, and Copinschi G

Subjects
Coma, Resuscitation, business.industry, General Medicine, Bemegride, Strychnine, Barbiturate Intoxication, chemistry.chemical_compound, Nikethamide, chemistry, Anesthesia, medicine, medicine.symptom, Amphetamine, business, medicine.drug, Picrotoxin
Abstract

After a short survey of the pharmacological properties of barbiturates and of the clinical signs of acute barbiturate intoxication, the authors review the different methods of treatment in use.Gast...

Published
1963

47. Syndrome De Budd-Chiari Par Cancer De La Surrenale

Author

Copinschi G, Arnould Y, and Malaisse-Lagae F

Subjects
Pathology, medicine.medical_specialty, business.industry, Cancer, General Medicine, medicine.disease, Inferior vena cava, Thrombosis, medicine.vein, Hepatic veins, cardiovascular system, medicine, Budd–Chiari syndrome, Adrenal Gland Cancer, business
Abstract

SummaryA case of adrenocortical virilizing cancer in a 32-year-okl woman is reported. Three months after the removal of the tumour, the patient developed a Budd-Chiari's syndrome secondary to neoplastic thrombosis of inferior vena cava and of hepatic veins.

Published
1967

48. Interrelations between sleep and the somatotropic axis.

Author

Van Cauter, E, Plat, L, and Copinschi, G

Abstract

In the human as in other mammals, growth hormone (GH) is secreted as a series of pulses. In normal young adults, a major secretory episode occurs shortly after sleep onset, in temporal association with the first period of slow-wave (SW) sleep. In men, approximately 70% of the daily GH output occurs during early sleep throughout adulthood. In women, the contribution of sleep-dependent GH release to the daily output is lower and more variable. Studies involving shifts of the sleep-wake cycle have consistently shown that sleep-wake homeostasis is the primary determinant of the temporal organization of human GH release. Effects of circadian rhythmicity may occasionally be detected. During nocturnal sleep, the sleep-onset GH pulse is caused by a surge of hypothalamic GHRH release which coincides with a circadian-dependent period of relative somatostatin disinhibition. Extensive evidence indicates the existence of a consistent relationship between SW sleep and increased GH secretion and, conversely, between awakenings and decreased GH release. There is a linear relationship between amounts of SW sleep--whether measured by visual scoring or by delta activity--and amounts of concomitant GH secretion, although dissociations may occur, most likely because of variable levels of somatostatin inhibition. Pharmacological stimulation of SW sleep results in increased GH release, and compounds which increase SW sleep may therefore represent a novel class of GH secretagogues. During aging, SW sleep and GH secretion decrease with the same chronology, raising the possibility that the peripheral effects of the hyposomatotropism of the elderly may partially reflect age-related alterations in sleep-wake homeostasis. While the association between sleep and GH release has been well documented, there is also evidence indicating that components of the somatotropic axis are involved in regulating sleep. The studies are most consistent in indicating a role for GHRH in promoting NREM and/or SW sleep via central, rather than peripheral, mechanisms. A role for GH in sleep regulation is less well-documented but seems to involve REM, rather than NREM, sleep. It has been proposed that the stimulation of GH release and the promotion of NREM sleep by GHRH are two separate processes which involve GHRH neurons located in two distinct areas of the hypothalamus. Somatostatinergic control of GH release appears to be weaker during sleep than during wake, suggesting that somatostatinergic tone is lower in the hypothalamic area(s) involved in sleep regulation and sleep-related GH release than in the area controlling daytime GH secretion. While the concept of a dual control of daytime and sleep-related GH secretion remains to be directly demonstrated, it allows for the reconciliation of a number of experimental observations.

Published
1998

49. EFFECTS OF TESTOSTERONE ON GONADOTROPHIN RESPONSES TO SYNTHETIC LH AND FSH RELEASING HORMONE (LRH) IN NORMAL MEN

Author

Robyn, C., L'Hermite, M., Leclercq, R., and Copinschi, G.

Abstract

LRH tests were performed in 6 adult men with intravenous injections of 25 μg, before and one week after an intramuscular injection of 250 mg testosterone oenanthate (Testoviron Depot®). One week after intramuscular injection of Testoviron the tonic secretion of LH was completely suppressed, but the reactivity or the reserve capacity of LH secretion, as tested by LRH, remained unchanged. In contrast, the tonic secretion of FSH and the reactivity of FSH secretion to LRH were both partly suppressed. Three months after the Testoviron injection, the basal levels of LH were still significantly lower than the control values, but the basal levels of FSH were identical to the control values. These data indicate that, in man, the feedback action of testosterone on gonadotrophin secretion could be exerted, at least for LH, at the hypothalamic level rather than at the pituitary level.No significant effects of LRH were noted on the circulating levels of growth hormone and sugar. There was a distinct rise in serum prolactin, which was occasionally significant, within 30 min after LRH injection; this is considered to be without physiological significance.

Published
1976
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50. Sleep loss results in an elevation of cortisol levels the next evening.

Author

Leproult, R, Copinschi, G, Buxton, O, and Van Cauter, E

Abstract

Sleep curtailment constitutes an increasingly common condition in industrialized societies and is thought to affect mood and performance rather than physiological functions. There is no evidence for prolonged or delayed effects of sleep loss on the hypothalamo-pituitary-adrenal (HPA) axis. We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels. Plasma cortisol profiles were determined during a 32-hour period (from 1800 hours on day 1 until 0200 hours on day 3) in normal young men submitted to three different protocols: normal sleep schedule (2300-0700 hours), partial sleep deprivation (0400-0800 hours), and total sleep deprivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sleep, plasma cortisol levels over the 1800-2300-hour period were similar on days 1 and 2. After partial and total sleep deprivation, plasma cortisol levels over the 1800-2300-hour period were higher on day 2 than on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss delays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation. Sleep loss could thus affect the resiliency of the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess.

Published
1997

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