Sleep apnea and its relationship with obesity and pre-diabetes
DOI:
https://doi.org/10.47196/diab.v57i3Sup.662Keywords:
apnea, prediabetes, obesityAbstract
Obstructive sleep apnea (OSA) is a highly prevalent condition with multiple associated comorbidities. Among them we find obesity, insulin resistance and diabetes, with a direct relationship between its severity and the degree of its complications. This entity generates with the successive cycles of obstruction and release of the upper airway (VAS), modifications in the autonomic nervous system, oxidative stress with activation of inflammation, release of chemical mediators and action on hormonal components that generate a pathological feedback loop with the aforementioned alterations1.
Obesity is perhaps the most important risk factor for the development of OSA. The prevalence of OSA in obese patients can be as high as 90% in those with morbid obesity. Weight gain has been seen to increase the Apnea/Hypopnea Index (AHI), while reducing it can improve the severity of OSA. The neck and the muscles of the upper airway are infiltrated with fat, decreasing its size and losing muscle tone, prone to collapse. OSA patients may have changes in the levels of leptin, ghrelin, adiponectin, hormones related to increased appetite and caloric intake. They also have insulin resistance and a decreased cardiac response to exercise, all factors that contribute to obesity2.
Regarding the role of OSA in the development of diabetes, it has been seen that intermittent hypoxia acts on the pancreas, causing a decrease in β cells, with greater apoptosis of the same, and in the liver, increasing glycogen deposits and increasing gluconeogenesis. Likewise, associated with the effects of sleep fragmentation, it generates insulin resistance by acting on the post-receptor, altering the GLUT4 transporters. Patients with DBT and neuropathy may favor OSA by acting on the upper airway nerves and the appearance of central apnea by acting at the level of the respiratory center3.
Treatment with CPAP, although it has been shown to improve leptin, orexin and neuropeptide Y levels, has not, so far, been shown to be effective in losing weight. Regarding their role in glucose metabolism, studies have been published with different results and it would seem that the time spent using these devices would be the key to improving metabolic control4.
References
I. Mesarwi OA, Sharma EV, Jun JC, Polotsky VY. Metabolic dysfunction in obstructive sleep apnea: a critical examination of underlying mechanisms. Sleep Biol Rhythms 2015 Jan;13(1):2-17. doi: 10.1111/sbr.12078.
II. Bonsignore MR, McNicholas WT, Montserrat JM, Eckel J. Adipose tissue in obesity and obstructive sleep apnoea. Eur Respir J 2012 Mar;39(3):746-67. doi: 10.1183/09031936.00047010.
III. Punjabi NM, Shahar E, Redline S, Gottlieb DJ, Givelber R, Resnick HE et al. Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study. Am J Epidemiol 2004;160(6):521-530.
IV. Pamidi S, Wroblewski K, Stepien M, Sharif-Sidi K, Kilkus J, Whitmore H, Tasali E. Eight hours of nightly continuous positive airway pressure treatment of obstructive sleep apnea improves glucose metabolism in patients with prediabetes. A randomized controlled trial. Am J Respir Crit Care Med 2015 Jul 1;192(1):96-105. doi: 10.1164/rccm.201408-1564OC.
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