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Polysomnographic Sleep, Growth Hormone Insulin‐like Growth Factor‐I Axis, Leptin, and Weight Loss
Author(s) -
Rasmussen Michael H.,
Wildschiødtz Gordon,
Juul Anders,
Hilsted Jannik
Publication year - 2008
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2008.249
Subject(s) - medicine , endocrinology , leptin , weight loss , obesity , insulin , growth hormone , insulin like growth factor , hormone , sleep (system call) , growth factor , receptor , computer science , operating system
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 μg/l; P < 0.01), and total‐IGF‐I (186 ± 21 vs. 301 ± 18 μg/l; P < 0.01) were significantly decreased and 24‐h leptin levels were increased (35 ± 5 vs. 12 ± 3 μg/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.