Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss

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Standard

Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss. / Rasmussen, Michael; Wildschiødtz, Gordon; Juul, Anders; Hilsted, Jannik.

I: Obesity, Bind 16, Nr. 7, 2008, s. 1516-1521.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Rasmussen, M, Wildschiødtz, G, Juul, A & Hilsted, J 2008, 'Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss', Obesity, bind 16, nr. 7, s. 1516-1521. https://doi.org/10.1038/oby.2008.249

APA

Rasmussen, M., Wildschiødtz, G., Juul, A., & Hilsted, J. (2008). Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss. Obesity, 16(7), 1516-1521. https://doi.org/10.1038/oby.2008.249

Vancouver

Rasmussen M, Wildschiødtz G, Juul A, Hilsted J. Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss. Obesity. 2008;16(7):1516-1521. https://doi.org/10.1038/oby.2008.249

Author

Rasmussen, Michael ; Wildschiødtz, Gordon ; Juul, Anders ; Hilsted, Jannik. / Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss. I: Obesity. 2008 ; Bind 16, Nr. 7. s. 1516-1521.

Bibtex

@article{bbe42ba0f83911ddb219000ea68e967b,
title = "Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss",
abstract = "Short sleep appears to be strongly associated with obesity and altered metabolic function, and sleep and growth hormone (GH) secretion seems interlinked. In obesity, both the GH-insulin-like-growth-factor-I (GH-IGF-I) axis and sleep have been reported to be abnormal, however, no studies have investigated sleep in relation to the GH-IGF-I axis and weight loss in obese subjects. In this study polygraphic sleep recordings, 24-h GH release, 24-h leptin levels, free-IGF-I, total-IGF-I, IGF-binding protein-3 (IGFBP-3), acid-labile subunit (ALS), cortisol and insulin sensitivity were determined in six severely obese subjects (BMI: 41+/-1 kg/m(2), 32+/-2 years of age), cross-sectional at baseline, and longitudinal after a dramatically diet-induced weight loss (36+/-7 kg). Ten age- and gender-matched nonobese subjects served as controls. Sleep duration (360+/-17 vs. 448+/-15 min/night; P<0.01), 24-h GH (55+/-9 vs. 344+/-55 mU/l.24 h; P<0.01), free-IGF-I (2.3+/-0.42 vs. 5.7+/-1.2 microg/l; P<0.01), and total-IGF-I (186+/-21 vs. 301+/-18 microg/l; P<0.01) were significantly decreased and 24-h leptin levels were increased (35+/-5 vs. 12+/-3 microg/l; P<0.01) in obese subjects at pre-weight loss compared with nonobese subjects After diet-induced weight loss the differences in GH, free IGF-I, and leptin were no longer present between previously obese and nonobese subjects, whereas a significant difference in sleep duration and total IGF-I levels persisted. Rapid eye movement (REM) sleep, non-REM sleep, IGFBP-3, ALS, and cortisol levels were similar in obese and nonobese subjects. Sleep duration, 24-h GH, and IGF-I levels were decreased and 24-h leptin levels were increased in obese subjects. We conclude that hyposomatotropism and hyperleptinemia in obesity are transient phenomena reversible with weight loss, whereas short sleep seems to persist after weight has been reduced dramatically Udgivelsesdato: 2008/7",
author = "Michael Rasmussen and Gordon Wildschi{\o}dtz and Anders Juul and Jannik Hilsted",
year = "2008",
doi = "10.1038/oby.2008.249",
language = "English",
volume = "16",
pages = "1516--1521",
journal = "Obesity",
issn = "1930-7381",
publisher = "Wiley-Blackwell",
number = "7",

}

RIS

TY - JOUR

T1 - Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss

AU - Rasmussen, Michael

AU - Wildschiødtz, Gordon

AU - Juul, Anders

AU - Hilsted, Jannik

PY - 2008

Y1 - 2008

N2 - Short sleep appears to be strongly associated with obesity and altered metabolic function, and sleep and growth hormone (GH) secretion seems interlinked. In obesity, both the GH-insulin-like-growth-factor-I (GH-IGF-I) axis and sleep have been reported to be abnormal, however, no studies have investigated sleep in relation to the GH-IGF-I axis and weight loss in obese subjects. In this study polygraphic sleep recordings, 24-h GH release, 24-h leptin levels, free-IGF-I, total-IGF-I, IGF-binding protein-3 (IGFBP-3), acid-labile subunit (ALS), cortisol and insulin sensitivity were determined in six severely obese subjects (BMI: 41+/-1 kg/m(2), 32+/-2 years of age), cross-sectional at baseline, and longitudinal after a dramatically diet-induced weight loss (36+/-7 kg). Ten age- and gender-matched nonobese subjects served as controls. Sleep duration (360+/-17 vs. 448+/-15 min/night; P<0.01), 24-h GH (55+/-9 vs. 344+/-55 mU/l.24 h; P<0.01), free-IGF-I (2.3+/-0.42 vs. 5.7+/-1.2 microg/l; P<0.01), and total-IGF-I (186+/-21 vs. 301+/-18 microg/l; P<0.01) were significantly decreased and 24-h leptin levels were increased (35+/-5 vs. 12+/-3 microg/l; P<0.01) in obese subjects at pre-weight loss compared with nonobese subjects After diet-induced weight loss the differences in GH, free IGF-I, and leptin were no longer present between previously obese and nonobese subjects, whereas a significant difference in sleep duration and total IGF-I levels persisted. Rapid eye movement (REM) sleep, non-REM sleep, IGFBP-3, ALS, and cortisol levels were similar in obese and nonobese subjects. Sleep duration, 24-h GH, and IGF-I levels were decreased and 24-h leptin levels were increased in obese subjects. We conclude that hyposomatotropism and hyperleptinemia in obesity are transient phenomena reversible with weight loss, whereas short sleep seems to persist after weight has been reduced dramatically Udgivelsesdato: 2008/7

AB - Short sleep appears to be strongly associated with obesity and altered metabolic function, and sleep and growth hormone (GH) secretion seems interlinked. In obesity, both the GH-insulin-like-growth-factor-I (GH-IGF-I) axis and sleep have been reported to be abnormal, however, no studies have investigated sleep in relation to the GH-IGF-I axis and weight loss in obese subjects. In this study polygraphic sleep recordings, 24-h GH release, 24-h leptin levels, free-IGF-I, total-IGF-I, IGF-binding protein-3 (IGFBP-3), acid-labile subunit (ALS), cortisol and insulin sensitivity were determined in six severely obese subjects (BMI: 41+/-1 kg/m(2), 32+/-2 years of age), cross-sectional at baseline, and longitudinal after a dramatically diet-induced weight loss (36+/-7 kg). Ten age- and gender-matched nonobese subjects served as controls. Sleep duration (360+/-17 vs. 448+/-15 min/night; P<0.01), 24-h GH (55+/-9 vs. 344+/-55 mU/l.24 h; P<0.01), free-IGF-I (2.3+/-0.42 vs. 5.7+/-1.2 microg/l; P<0.01), and total-IGF-I (186+/-21 vs. 301+/-18 microg/l; P<0.01) were significantly decreased and 24-h leptin levels were increased (35+/-5 vs. 12+/-3 microg/l; P<0.01) in obese subjects at pre-weight loss compared with nonobese subjects After diet-induced weight loss the differences in GH, free IGF-I, and leptin were no longer present between previously obese and nonobese subjects, whereas a significant difference in sleep duration and total IGF-I levels persisted. Rapid eye movement (REM) sleep, non-REM sleep, IGFBP-3, ALS, and cortisol levels were similar in obese and nonobese subjects. Sleep duration, 24-h GH, and IGF-I levels were decreased and 24-h leptin levels were increased in obese subjects. We conclude that hyposomatotropism and hyperleptinemia in obesity are transient phenomena reversible with weight loss, whereas short sleep seems to persist after weight has been reduced dramatically Udgivelsesdato: 2008/7

U2 - 10.1038/oby.2008.249

DO - 10.1038/oby.2008.249

M3 - Journal article

C2 - 18464752

VL - 16

SP - 1516

EP - 1521

JO - Obesity

JF - Obesity

SN - 1930-7381

IS - 7

ER -

ID: 10453426