Sleep-disordered breathing is a prevalent condition associated with impairment of daytime function and may predispose individuals to metabolic abnormalities independent of obesity. The primary objective of this study was to determine the metabolic consequences and community prevalence of sleep-disordered breathing in mildly obese, but otherwise healthy, individuals. One hundred and fifty healthy men, without diabetes or cardiopulmonary disease, were recruited from the community. Measurements included polysomnography, a multiple sleep latency test, an oral glucose tolerance test, determination of body fat by hydrodensitometry, and fasting insulin and lipids. The prevalence of sleep-disordered breathing, depending on the apnea-hypopnea index (AHI) cutoff, ranged from 40 to 60%. After adjusting for body mass index (BMI) and percent body fat, an AHI gt-or-equal, slanted 5 events/h was associated with an increased risk of having impaired or diabetic glucose tolerance (odds ratio, 2.15; 95% CI, 1.05-4.38). The impairment in glucose tolerance was related to the severity of oxygen desaturation (DeltaSa(O(2))) associated with sleep-disordered breathing. For a 4% decrease in oxygen saturation, the associated odds ratio for worsening glucose tolerance was 1.99 (95% CI, 1.11 to 3.56) after adjusting for percent body fat, BMI, and AHI. Multivariable linear regression analyses revealed that increasing AHI was associated with worsening insulin resistance independent of obesity. Thus, sleep-disordered breathing is a prevalent condition in mildly obese men and is independently associated with glucose intolerance and insulin resistance.

Pima subjects homozygous for the Trp64Arg beta 3-adrenergic-receptor mutation have an earlier onset of NIDDM and tend to have a lower resting metabolic rate. This mutation may accelerate the onset of NIDDM by altering the balance of energy metabolism in visceral adipose tissue.

EMIPARESIS REPRESENTS THE dominant functionally limiting symptom in 80% of patients with acute stroke. 1 Within 2 to 5 months after a stroke, patients recover a variable degree of function, depending on the magnitude of the initial deficit. 1 Several studies have demonstrated that recovery is associated with reorganization of central nervous system networks. 2,3 Functional brain imaging of paretic movement during the recovery period has shown recruitment of cortex immediately adjacent to the stroke cavity along with intact cortical areas within the lesioned and in the uninjured contralesional hemisphere. 4,5 The pattern of recruitment depends on the severity of impairment, 6 lesion location, 7 and time since stroke. 8 The factors that initiate and maintain cortical reorganization are not known. Imaging data suggest that circuitry in motor cortices on both sides of the brain is modified during recovery. 2