The influence of obstructive sleep apnea on the expression of glycerol-3-phosphate dehydrogenase1 gene

Glycerol-3-phosphate dehydrogenase1 ( GPD1) is considered to be a key enzyme that connects carbohydrate and lipid metabolism. This gene is induced in response to sleep deprivation, suggesting a potential role for this enzyme in the manifestation of obstructive sleep apnea (OSA). This study aims to examine the effects of sleep apnea, obesity and other relevant clinical parameters on GPD1 expression in the peripheral blood of a rigorously selected sample population in order to identify a biological marker that would allow for early intervention and prevention of the disorder. Clinical and sleep parameters were assessed by a complete full-night polysomnography and the expression of GPD1 at the mRNA level was determined. The results were compared among 20 OSA patients and 20 controls, further classified into two subgroups according to their body mass index. The expression levels of the GPD1 gene did not differ between patients with OSA and their matched controls. The results were not affected by the clinical and biochemical measurements, the sleep parameters or the severity of nocturnal hypoxemia. On the other hand, individuals with OSA had higher levels of fasting glucose when compared with weight-matched controls ( P = 0.01). Moreover, higher very low-density lipoprotein (VLDL) was found in the over-weight OSA patient group, and higher cholesterol levels were found in the eutrophic OSA group when compared with their respective controls ( P < 0.05). Based on logistic regression analyses, fasting glucose levels emerged as an independent factor for OSA in both the eutrophic (odds ratio [OR] = 1.27; 95% confidence interval [CI] = 1.00–1.59) and over-weight groups (OR = 1.29; 95% CI = 1.04–1.59). Although the results from the current study corroborate the growing body of data connecting OSA to altered glucose metabolism, it does not provide evidence for the modulation of GPD1 transcription by either OSA or its related phenotypes. This suggests that GPD1 may not play a major role in the OSA manifestation.