Heart in Diabetes

Heart in Diabetes


Punjabi N. OSA, hyperglycemia and diabetes. Presented at: Heart in Diabetes Annual Meeting; Sept. 10-12, 2021 (hybrid meeting).

Disclosures: Punjabi reports no relevant financial disclosures.
September 14, 2021
3 min read

Metabolic consequences of obstructive sleep apnea persist, despite treatment


Punjabi N. OSA, hyperglycemia and diabetes. Presented at: Heart in Diabetes Annual Meeting; Sept. 10-12, 2021 (hybrid meeting).

Disclosures: Punjabi reports no relevant financial disclosures.
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Obstructive sleep apnea can predispose a person to hyperglycemia and even type 2 diabetes, yet data show continuous positive airway pressure therapy does not improve markers of glucose dysregulation, according to a speaker.

Independent of total body fat, obstructive sleep apnea (OSA) is associated with impaired glucose disposal and may also impair the compensatory response in insulin secretion for a given degree of insulin resistance, Naresh M. Punjabi, MD, PhD, chief of the division of pulmonary, critical care and sleep medicine at the University of Miami Miller School of Medicine, said during a presentation at the Heart in Diabetes CME conference. OSA also seems to impair insulin independent of glucose uptake and is associated with altered free fatty acid kinetics, independent of BMI and body fat, Punjabi said.

Woman using CPAP
Source: Adobe Stock.

“What we are putting forth during the last decades [of research] is that sleep apnea, through its effects of hypoxemia, may induce insulin resistance and accelerate betacell compensation to that insulin resistance,” Punjabi said.

Role of OSA in glucose intolerance

Naresh M. Punjabi, MD, PhD

Cross-sectional and observational studies dating back to the early 1990s demonstrated that adults with OSA or those who snore were more likely to have impaired glucose tolerance, though data were limited at the time, Punjabi said. A pivotal shift occurred in 2004 when the Sleep Heart Health Study, one of the largest longitudinal studies assessing sleep apnea and cardiovascular disease, provided data on glucose metabolism.

“What we learned from that study is if you looked at prevalence of impaired or diabetic fasting glucose, you saw a dose-response relationship between the severity of sleep apnea and the prevalence of these two metabolic abnormalities,” Punjabi said. “Among those without sleep apnea compared with those with mild or moderate to severe sleep apnea, there was a graded increase in the prevalence, going from about 8% to about 18%, adjusting for things such as obesity and other CV risk factors. Not only was sleep apnea associated with impaired fasting glucose, the key finding was the degree of hypoxemia, as indexed by the average oxygen saturation during sleep, was also associated with fasting hyperglycemia.”

Data also show lower oxygen saturation during sleep was associated with lower homeostatic model assessment, a method of assessing beta-cell function in insulin resistance, he said. Limited data also suggest OSA is associated with impaired insulin secretion.

“Sleep apnea and altered glucose metabolism, no matter how you summarize — metrics of insulin sensitivity, prevalence of metabolic syndrome, prevalence of type 2 diabetes — all are associated with sleep apnea severity.”

CPAP therapy ineffective

Currently, there is not sufficient evidence from randomized controlled trials to suggest HbA1c or other metrics of glycemic response improve with as a treatment for OSA, Punjabi said.

“Does the treatment of sleep apnea with CPAP therapy, which is a first-line [treatment], improve glucose homeostasis?” Punjabi said. “The answer to that is, no, not right now. We know there is observational data that HbA1c, after CPAP, is lower. This data from almost 15 years ago led to a great level of interest in whether treating sleep apnea would improve glycemic control. Unfortunately, we have not found that to be the case.”

Punjabi suggested that limits in study design may explain why data from randomized clinical trials assessing CPAP therapy in OSA do not support what is seen in animal and experimental models.

“The problem is our studies are very limited in size,” Punjabi said. “We have a lot of static measures, like HbA1c, and haven’t looked at other metrics like insulin secretion. We have very minimal duration of OSA therapy — maybe 3 months, 6 months. We have a very difficult issue with compliance with CPAP therapy. Often our [participants] have varying degrees of metabolic disease, and there is potential for reversibility.”

Animal models suggest that, under controlled hypoxic conditions, fasting hyperglycemia develops, and improves with normoxia.

“That is only half the story,” Punjabi said. “If you perform a glucose tolerance test, the curves do not return to normal. That suggests to us that there may be an irreversible component if we do not intervene early.”