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1 Division of Clinical and Administrative Pharmacy, College of Pharmacy, and 3 Department of Internal Medicine, College of Medicine, University of Iowa, Iowa City, Iowa 52242; 2 Department of Hypertension and Diabetology, Medical University of Gdansk, Gdansk, Poland; and 4 Division of Hypertension and Division of Cardiovascular Disease, Department of Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905
Patients with obstructive sleep apnea
(OSA) are frequently obese and are predisposed to weight gain. They
also have heightened sympathetic drive. We reasoned that noradrenergic
activation of
3-receptors on adipocytes would inhibit
leptin production, predisposing to obesity in sleep apnea. We therefore
tested the hypothesis that obesity and predisposition to weight gain in
OSA are associated with low levels of plasma leptin. We prospectively
studied 32 male patients (43 ± 2 yr) with OSA who were newly
diagnosed and never treated and who were free of any other diseases.
Control measurements were obtained from 32 similarly obese closely
matched male subjects (38 ± 2 yr). Leptin levels were 13.7 ± 1.3 and 9.2 ± 1.2 ng/ml in patients with OSA and controls,
respectively (P = 0.02). Weight gain over the year
before diagnosis was 5.2 ± 1.7 and 0.5 ± 0.9 kg in sleep
apnea patients and similarly obese control subjects, respectively
(P = 0.04). Muscle sympathetic activity was 46 ± 4 and 30 ± 4 bursts/min in patients with OSA (n = 16) and control subjects (n = 18), respectively
(P = 0.01). Plasma leptin levels are elevated in newly
diagnosed otherwise healthy patients with untreated sleep apnea beyond
the levels seen in similarly obese control subjects without sleep
apnea. Higher leptin levels in OSA, independent of body fat content, suggest that OSA is associated with resistance to the weight-reducing effects of leptin.
obesity; heart rate; sympathetic nervous system
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