OBJECTIVES: to investigate the association of sleep apnea severity with insulin resistance, leptin, adipose-fatty acid binding protein (A-FABP) and visfatin levels and to evaluate the confounding role of obesity. STUDY DESIGN: prospective study. METHODS: the study included obese patients who were referred to the sleep laboratory. Patients were divided into two main groups according to their Apnea-Hypopnea Index (AHI). Measurements of body weight, height, blood pressure, waist circumference (WC), and neck circumference (NC) were taken on the night of the sleep study. Blood samples were taken after polysomnography. Insulin resistance was estimated with the homeostasis model assessment (HOMA) index. RESULTS: group A included 34 patients with obstructive sleep apnea syndrome (OSAS) and group B included 19 patients without OSAS. OSAS patients had significant higher visfatin levels; however, other parameters were similar. Leptin and A-FABP were significantly correlated with body mass index (BMI) in both groups. OSAS patients had significant higher NC and WC despite a BMI similar to that of group B, and strong correlations of these two variables were found with HOMA. Group A had higher visfatin levels than did group B. CONCLUSIONS: insulin resistance was not directly associated with BMI and/or AHI, but it was aggravated by nocturnal hypoxemia owing to apnea severity. NC was also a good predictor for insulin resistance and should not be ignored during the treatment selection for the patients with OSAS. Visfatin may have a potential role as a screening marker for OSAS.
OBJECTIVES: to investigate the association of sleep apnea severity with insulin resistance, leptin, adipose-fatty acid binding protein (A-FABP) and visfatin levels and to evaluate the confounding role of obesity. STUDY DESIGN: prospective study. METHODS: the study included obesepatients who were referred to the sleep laboratory. Patients were divided into two main groups according to their Apnea-Hypopnea Index (AHI). Measurements of body weight, height, blood pressure, waist circumference (WC), and neck circumference (NC) were taken on the night of the sleep study. Blood samples were taken after polysomnography. Insulin resistance was estimated with the homeostasis model assessment (HOMA) index. RESULTS: group A included 34 patients with obstructive sleep apnea syndrome (OSAS) and group B included 19 patients without OSAS. OSAS patients had significant higher visfatin levels; however, other parameters were similar. Leptin and A-FABP were significantly correlated with body mass index (BMI) in both groups. OSAS patients had significant higher NC and WC despite a BMI similar to that of group B, and strong correlations of these two variables were found with HOMA. Group A had higher visfatin levels than did group B. CONCLUSIONS:insulin resistance was not directly associated with BMI and/or AHI, but it was aggravated by nocturnal hypoxemia owing to apnea severity. NC was also a good predictor for insulin resistance and should not be ignored during the treatment selection for the patients with OSAS. Visfatin may have a potential role as a screening marker for OSAS.