Results: Waist circumference, waist-to-hip ratio (WHR), and US-determined visceral fat values showed the best correlation coefficients with visceral fat determined by CT (r ϭ 0.55, 0.54, and 0.71, respectively; p Ͻ 0.01). Fat mass determined by DXA was inversely correlated with visceralto-subcutaneous-fat ratio (r ϭ Ϫ0.47, p Ͻ 0.01). Bioimpedance-determined fat mass and skinfolds were correlated with only subcutaneous abdominal fat quantified by CT. Linear regression indicated US visceral-fat distance and WHR as the main predictors of CT-determined visceral fat (adjusted r 2 ϭ 0.51, p Ͻ 0.01). A waist measurement of 107 cm (82.7% specificity, 60.6% sensitivity) and WHR of 0.97 (78.8% specificity, 63.8% sensitivity) were chosen as discriminator values corresponding with visceral obesity diagnosed by CT. A value of 6.90 cm for visceral fat USdetermined diagnosed visceral obesity with a specificity of 82.8%, a sensitivity of 69.2%, and a diagnostic concordance of 74% with CT.Discussion: US seemed to be the best alternative method for the assessment of intra-abdominal fat in obese women. Its diagnostic value could be optimized by an anthropometric measurement. Prospective studies are needed to establish CT and US cutoffs for defining visceral-fat levels related to elevated cardiovascular risk.

Abstract-Visceral fat accumulation is associated with increased cardiovascular risk. Clinical evaluation of visceral fat is limited because of the lack of reliable and low-cost methods. To assess the correlation between ultrasonography and computed tomography (CT) for the evaluation of visceral fat, 101 obese women, age 50.5Ϯ7.7 years with a body mass index of 39.2Ϯ5.4 kg/m 2 , were submitted to ultrasonograph and CT scans. Visceral fat measured by ultrasonography, 1 cm above the umbilical knot, showed a high correlation with CT-determined visceral fat (rϭ0.67, PϽ0.0001). The ultrasonograph method showed good reproducibility with an intra-observer variation coefficient of Ͻ2%. Both ultrasonograph and CT visceral fat values were correlated with fasting insulin (rϭ0.29 and rϭ0.27, PϽ0.01) and plasma glucose 2 hours after oral glucose load (rϭ0.22 and rϭ0.34, PϽ0.05), indicating that ultrasonography is a useful method to evaluate cardiovascular risk. A significant correlation was also found between visceral fat by CT and serum sodium (rϭ0.18, PϽ0.05). A ultrasonograph-determined visceral-to-subcutaneous fat ratio of 2.50 was established as a cutoff value to define patients with abdominal visceral obesity. This value also identified patients with higher levels of plasma glucose, serum insulin and triglycerides and lower levels of HDL-cholesterol, which are metabolic abnormalities characteristic of the metabolic syndrome. Our data demonstrate that ultrasonography is a precise and reliable method for evaluation of visceral fat and identification of patients with adverse metabolic profile.

Obesity is a well-known risk factor for the development of insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease. Rather than the total amount of fat, central distribution of adipose tissue is very important in the pathophysiology of this constellation of abnormalities termed metabolic syndrome. Adipose tissue, regarded only as an energy storage organ until the last decade, is now known as the biggest endocrine organ of the human body. This tissue secretes a number of substances--adipocytokines--with multiple functions in metabolic profile and immunological process. Therefore, excessive fat mass may trigger metabolic and hemostatic disturbances as well as CVD. Adipocytokines may act locally or distally as inflammatory, immune or hormonal signalers. In this review we discuss visceral obesity, the potential mechanisms by which it would be related to insulin resistance, methods for its assessment and focus on the main adipocytokines expressed and secreted by the adipose tissue. Particularly, we review the role of adiponectin, leptin, resistin, angiotensinogen, TNF-alpha, and PAI-1, describing their impact on insulin resistance and cardiovascular risk, based on more recent findings in this area.

Sympathetic nervous system and hypothalamic-pituitary-adrenal (HPA) axis activation may be the mechanism of this relationship. The aim of this study was to evaluate HPA axis and ambulatory blood pressure monitoring in obese men with and without OSAS and to determine whether nasal continuous positive airway pressure therapy (nCPAP) influenced responses. Twenty-four-hour ambulatory blood pressure monitoring and overnight cortisol suppression test with 0.25 mg of dexamethasone were performed in 16 obese men with OSAS and 13 obese men controls. Nine men with severe apnea were reevaluated 3 mo after nCPAP therapy. Body mass index and blood pressure of OSAS patients and obese controls were similar. In OSAS patients, the percentage of fall in systolic blood pressure at night (P ϭ 0.027) and salivary cortisol suppression postdexamethasone (P ϭ 0.038) were lower, whereas heart rate (P ϭ 0.022) was higher compared with obese controls. After nCPAP therapy, patients showed a reduction in heart rate (P ϭ 0.036) and a greater cortisol suppression after dexamethasone (P ϭ 0.001). No difference in arterial blood pressure (P ϭ 0.183) was observed after 3 mo of nCPAP therapy. Improvement in cortisol suppression was positively correlated with an improvement in apnea-hypopnea index during nCPAP therapy (r ϭ 0.799, P ϭ 0.010). In conclusion, men with OSAS present increased postdexamethasone cortisol levels and heart rate, which were recovered by nCPAP. sleep disorders; low-dose dexamethasone test; ambulatory blood pressure monitoring OBSTRUCTIVE SLEEP APNEA SYNDROME (OSAS) is receiving increased attention because it seems to be associated with a variety of long-term consequences, such as high rates of morbidity and mortality, mostly due to cardiovascular disease (23). Although obesity is the main risk factor for OSAS (39), it has been demonstrated that OSAS may increase the risk for hypertension, myocardial infarction, congestive heart failure, and stroke independently of obesity. Continuous positive airway pressure (CPAP) therapy is the treatment of choice for patients with moderate-to-severe OSAS, since it is highly effective in improving nocturnal hypoxia and sleep fragmentation, enhancing the quality of life and reducing many cardiovascular complications related to OSAS. However, the lack of acceptance and inadequate adherence to CPAP therapy remain the major causes of sleep apnea treatment failure (10,20,21,31,32).The mechanisms proposed to explain the increased cardiovascular disease in obstructive sleep apnea are under assessment. It is speculated that recurrent episodes of upper airway constriction, progressive hypoxemia, and sleep fragmentation may result in neural and metabolic changes, including activation of peripheral sympathetic activity, inflammatory pathways, and hypothalamic-pituitary-adrenal (HPA) axis, impairment of insulin sensitivity, and generation of reactive oxygen species, which could predispose to vascular damage (16,26,27,34).Sympathetic nervous system has been well demonstrated to be activated in sleep ap...

nCPAP therapy reverses hypoadiponectinemia levels present in obese men with OSA, probably through reductions in hypoxia and inflammation activity.