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Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss.
Obesity (Silver Spring). 2008 Jul; 16(7):1516-21.O

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.

Authors+Show Affiliations

Department of Endocrinology, Hvidovre Hospital, University of Copenhagen, Hvidovre, Denmark. mhr@dadlnet.dkNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Controlled Clinical Trial
Journal Article

Language

eng

PubMed ID

18464752

Citation

Rasmussen, Michael H., et al. "Polysomnographic Sleep, Growth Hormone Insulin-like Growth factor-I Axis, Leptin, and Weight Loss." Obesity (Silver Spring, Md.), vol. 16, no. 7, 2008, pp. 1516-21.
Rasmussen MH, Wildschiødtz G, Juul A, et al. Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss. Obesity (Silver Spring). 2008;16(7):1516-21.
Rasmussen, M. H., Wildschiødtz, G., Juul, A., & Hilsted, J. (2008). Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss. Obesity (Silver Spring, Md.), 16(7), 1516-21. https://doi.org/10.1038/oby.2008.249
Rasmussen MH, et al. Polysomnographic Sleep, Growth Hormone Insulin-like Growth factor-I Axis, Leptin, and Weight Loss. Obesity (Silver Spring). 2008;16(7):1516-21. PubMed PMID: 18464752.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss. AU - Rasmussen,Michael H, AU - Wildschiødtz,Gordon, AU - Juul,Anders, AU - Hilsted,Jannik, Y1 - 2008/05/08/ PY - 2008/5/10/pubmed PY - 2008/9/16/medline PY - 2008/5/10/entrez SP - 1516 EP - 21 JF - Obesity (Silver Spring, Md.) JO - Obesity (Silver Spring) VL - 16 IS - 7 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. SN - 1930-7381 UR - https://www.unboundmedicine.com/medline/citation/18464752/Polysomnographic_sleep_growth_hormone_insulin_like_growth_factor_I_axis_leptin_and_weight_loss_ L2 - https://doi.org/10.1038/oby.2008.249 DB - PRIME DP - Unbound Medicine ER -