Increased resting energy expenditure and insulin resistance in male patients with moderate-to severe obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) has been associated with disturbances in energy metabolism and insulin resistance, nevertheless, the links between OSA severity, resting energy expenditure (REE) and insulin resistance (homeostasis model assessment, HOMA-IR) remained unexplored. Therefore, we investigated the effects of OSA severity on REE, and relationships between REE and HOMA-IR in patients with OSA. Forty men [mean (SD) age 49.4 (11.4) years] underwent overnight polysomnography; REE was assessed using indirect calorimetry. REE adjusted for fat-free mass (FFM) was higher in patients with moderate-to severe OSA [n=24; body mass index (BMI) 31.1 (2.7) kg.m(-2); apnoea-hypopnoea index (AHI)>/=15 episodes.h(-1)] compared to participants with no clinically significant OSA (n=16; BMI 30.3 (2.2) kg.m(-2); AHI<15 episodes.h(-1)) [median (interquartile range) 30.4 (26.1-31.3) versus 25.8 (24.6-27.3) kcal.kg(-1).24 h(-1), p=0.005)]. AHI and oxygen desaturation index (ODI) were directly related to REE/FFM (p=0.001; p<0.001, respectively) and to HOMA-IR (p<0.001 for both). In stepwise multiple linear models, REE/FFM was independently predicted by ODI (p<0.001) and age (p=0.028) (R(2)=0.346); HOMA-IR was independently predicted by ODI only (p<0.001, R(2)=0.457). In conclusion, male patients with moderate-to severe OSA have increased REE paralleled by impaired insulin sensitivity. Severity of nocturnal intermittent hypoxia reflected by ODI is an independent predictor of REE/FFM and HOMA-IR.

Circulatory and adipose tissue leptin and adiponectin in relationship to resting energy expenditure in patients with chronic obstructive pulmonary disease.

Increases in resting energy expenditure (REE) likely contribute to weight loss in various chronic diseases. In chronic obstructive pulmonary disease (COPD), relationships between the ventilatory impairment and increased REE, and between disturbances in adipokines and weight loss were previously described. Therefore, we investigated serum levels and adipose tissue expression of leptin and adiponectin, and their relationships to REE in patients with COPD. In 44 patients with stable COPD (38 male; age 62.3+/-7.2 years), REE was assessed using indirect calorimetry. Subcutaneous adipose tissue samples were analyzed using real-time PCR. From underweight [n=9; body mass index (BMI) <20.0 kg.m(-2)], to normal weight-overweight (n=24, BMI=20.0-29.9 kg.m(-2)) and obese patients (n=11; BMI>/=30 kg.m(-2)), REE adjusted for body weight decreased (32.9+/-6.1 vs. 26.2+/-5.8 vs. 23.9+/-6.6 kcal.kg(-1).24 h(-1), p=0.006), serum levels and adipose tissue expression of leptin increased (p<0.001 for both), and serum and adipose tissue adiponectin decreased (p<0.001; p=0.004, respectively). REE was inversely related to serum and adipose tissue leptin (R=-0.547, p<0.001; R=-0.458, p=0.002), and directly to serum adiponectin (R=0.316, p=0.039). Underweight patients had increased REE compared to normal weight-overweight patients, in association with reductions in serum and adipose tissue leptin, and increased serum adiponectin, suggesting a role of adipokines in energy imbalance in COPD-related cachexia.