BACKGROUND: Insulin resistance (IR) and progressive pancreatic β-cell dysfunction have been identified as the two fundamental features in the pathogenesis of obesity and non-insulin-dependent diabetes mellitus. We aimed to investigate correlations between anthropometric indices of obesity and IR in nondiabetic obese individuals, and the cutoff value from receiver operating characteristic (ROC) curve analysis. DESIGN AND SETTING: Cross-sectional study conducted in a private clinic. METHODS:We included obese individuals (body mass index, BMI ≥ 30 kg/m 2 ) with no diabetes mellitus (fasting glucose levels ≤ 126 mg/dl). The participants were evaluated for the presence of cardiovascular risk factors and through anthropometric measurements and biochemical tests. Furthermore, IR was assessed indirectly using the homeostatic model assessment (HOMA)-IR and HOMA-β indexes. The area under the curve (AUC) of the variables was compared. The sensitivity, specificity and cutoff of each variable for diagnosing IR were calculated. RESULTS: The most promising anthropometric parameters for indicating IR in non-diabetic obese individuals were waist-to-height ratio (WHtR), waist circumference (WC) and BMI. WHtR proved to be an independent predictor of IR, with risk increased by 0.53% in HOMA-IR, 5.3% in HOMA-β and 1.14% in insulin.

Sleep loss has been implicated in triggering the hypertension. The goal of the present study was investigated the possible mechanisms underlying cardiovascular alterations after acute paradoxical sleep deprivation (PSD). Male Wistar rats were assigned in two experimental groups: (1) control and (2) PSD for 24 h using the modified single platform method. Paradoxical sleep deprived rats exhibited higher blood pressure, heart rate (HR) and impaired baroreceptor sensitivity. After pharmacological autonomic double blockade (propranolol and methylatropine administration), intrinsic heart rate was decreased after PSD. The PSD rats showed a reduction in the vagal tone without affecting sympathetic tone. Isoproterenol administration (0.001, 0.01 and 1 µg/kg) induced an increase in ΔHR responses in PSD group. Electrocardiographic analysis in response to β-adrenergic stimulation indicated that PSD contributed to ventricular cardiac arrhythmias. Our findings suggest that acute paradoxical sleep loss induce cardiovascular alterations, autonomic imbalance accompanied by impaired baroreflex sensitivity and increased arrhythmia susceptibility.

No abstract

No abstract

No abstract