We conclude that while insulin and leptin action may contribute to the development of OSA, further research is required to determine the mechanistic actions and relative contributions independent of body weight.
This study examined the association between depressive symptoms, as well as depressive symptom dimensions, and three candidate biological pathways linking them to Obstructive sleep apnea (OSA): (1) inflammation; (2) circulating leptin; and (3) intermittent hypoxemia.
The potential associations of leptin and leptin receptor (LEPR) polymorphisms with OSA have been studied in different populations; however, the results remain inconclusive.
The effect of leptin on the pathophysiology of obstructive sleep apnea is being investigated, but the results of studies have been confounded by leptin's diurnal variation and the short-term effects of feeding, adiposity, age, and sex.
The aim of this study was to compare serum leptin, apolipoprotein A1 (ApoA1), apolipoprotein J (ApoJ) and apolipoprotein H (ApoH) levels in males with obstructive sleep apnea and hypopnea syndrome (OSAHS) to those in healthy control subjects and to examine the possible relation between neurocognitive performance and these factors/serum markers in the subjects.
Serum levels of leptin, macrophage migration inhibitory factor (MIF), interleukin-6 (IL-6), high sensitive C-reactive protein (Hs-CRP), and tumor necrosis factor alpha (TNF-α) were significantly higher, and adiponectin levels were significantly lower in OSA with NAFLD subjects.
Our study suggested that leptin and LEPR polymorphisms had no association with OSA risk in all examined patients, whereas there was an association between Gln233Arg polymorphism and OSA risk in Europeans.
Our review of the published literature suggests that leptin levels seem to correlate with body mass index and adiposity rather than obstructive sleep apnea.
In this study, we identified the variables that predict BP response to CPAP.24-h ambulatory BP monitoring (ABPM), C-reactive protein (CRP), leptin, adiponectin and 24-h urinary catecholamine were measured before and after 6 months of CPAP in obstructive sleep apnoea (OSA) patients.Overall, 88 middle-aged, obese male patients with severe OSA (median apnoea-hypopnoea index 42 events·h<sup>-1</sup>) were included; 28.4% had hypertension.
Four significant risk factors for OSA were identified: maternal obesity/diabetes during pregnancy (OR, 1.63; 95% CI, 1.21-2.21; P = .001), preterm/low birth weight (OR, 1.74; 95% CI, 1.30-2.32; P < .001), early childhood obesity (OR, 1.89; 95% CI, 1.37-2.62; P < .001), and high leptin levels in early childhood (OR, 1.94; 95% CI, 1.22-3.09; P = .005).
Chronic hyperinsulinemia due to insulin resistance, high plasma levels of leptin, and/or obstructive sleep apnea may be responsible for sympathetic overactivity in obesity-related hypertension.
Leptin levels were higher in the mild to moderate OSAS group (23.1+/-21.8 ng/ml, p<0.05) and in the severe OSAS group (20.2+/-17.5 ng/ml, p<0.05) than in the non-OSAS group (9.4+/-6.4 ng/ml).