Detalle Publicación

ARTÍCULO
Hyperleptinemia and insulinresistance in obesity-associated sleep apnoea: Sex-dependent effects of CPAP application
Título de la revista: ENDOCRINE ABSTRACTS
ISSN: 1470-3947
Volumen: 35
Fecha de publicación: 2014
Resumen:
Obstructive sleep apnoea (OSA) is very common in severe obese patients and has been related to insulin resistance (IR) and hyperleptinemia, and these findings may have effects on food behavior and obesity complications. In order to explore this relationship and the role of sex we have studied 531 patients with morbid obesity (BMI 42.8+6.5 kg/m2). A full polysomnographic study and glucose, insulin and leptin measurements as well as air displacement plethysmography were performed in all of them. Ninety-six obese patients (BMI 45,8+7.3 kg/m2) with OSA were evaluated before and immediately after nocturnal CPAP treatment for 24 h. About 370 out of 531 patients had OSA (AHI 37.7+28/h). OSA patients had higher glucose (108+29 vs 99+26 mg/dl.P<0.001), insulin plasma levels (20+12 vs 16+10 (mu/l.P<0.001) and HOMA index (HOMAi) values (5.5+4.1 vs 4+2.8.P<0.001), but lower leptin levels (45.4+27 vs 55.5+28 ng/ml.P<0.001) and lower fat mass (48.9+7.5 vs 50.5+6.6%.P<0.05) than non-OSA patients. When compared with basal conditions, as a whole group (n=96) CPAP administration was followed by a reduction in glucose (108.3+29.4 vs 115+33.7.P<0.001), and insulin values (21.4+16.4 vs 23.8+16.3 mU/l.P<0.01) without any change in leptin concentrations (49.9+31.3 vs 50+32.3 mU/l. P=NS). Male patients (n=52) showed reductions in glucose values (109.1+22.3 vs 116+26.3 mg/dl.P<0.01) and HOMAi (5.8+3.2 vs 7+4.9.P<0.05). However, no changes either in glucose (PreM: 112+49.7 vs 114+52 mg/dl.P=NS), insulin values or HOMAi (5.1+3.9 vs 6.4+4.8.P=NS) were seen in PreM women following CPAP. In contrast, postmenopausal women (PostM; n=21) showed a reduction in glucose (102.9+17.8 vs 113+28.8 mg/dl.P<0.01), insulin (18.1+11.3 vs 23.5+17.5 mU/L.P<0.05) and HOMAi (4.9+4.2 vs 7.1+8.1.P<0.05) with no variation in leptin values (67+25.3 vs 65+31.9 ng/ml.P=NS) after CPAP. There was no correlation between reduction in apnoea index and decrease in HOMA index after CPAP in any of the subgroups. These data indicate that either OSA in itself or its correction by CPAP has no effects on leptin secretion in patients with morbid obesity. Globally, OSA potentiates IR, but acute correction of OSA by CPAP has more beneficial effects in PostM women and men than in PreM women.