Obstructive sleep apnoea and type 1 diabetes mellitus

Tan, Hiang Leng; Babwah, Feaz; Waheed, Najeeb; Butt, Muhammad Imran

doi:10.15277/bjdvd.2015.020

Cited by 1 publication

(1 citation statement)

References 12 publications

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“…Therefore, whether the negative association of T2DM with OSA, and vice versa, is independent of adiposity or arises as a consequence of it remains unclear [ 5 , 40 ]. An unexpectedly high prevalence of OSA (40%) in non-obese type 1 diabetic individuals, not dissimilar to that of type 2 diabetic individuals (23–50%), however, implies that hyperglycaemia and glucose dysmetabolism may increase susceptibility to or accelerate progression of OSA [ 5 , 41 ]. In a 4-month-long small (n = 24) interventional study investigating whether glycaemic control optimisation therapy in type 2 diabetic individuals impacted sleep breathing parameters, Guiterrez-Carrasguilla et al demonstrated that participants with a HbA1c reduction ≥0.5% had significant improvements in the AHI (26.1 (8.6 to 95.0) events/h at baseline vs. 20.0 (4.0 to 62.4) events/h at the end) [ 42 ].…”

Section: Osa Hyperglycaemia and Diabetes Mellitusmentioning

confidence: 99%

Metabolic Crossroads: Unveiling the Complex Interactions between Obstructive Sleep Apnoea and Metabolic Syndrome

Heffernan,

Duplancic,

Kumric

et al. 2024

IJMS

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Obstructive sleep apnoea (OSA) and components of metabolic syndrome (MetS) are inextricably connected. Considering the increasing burden of MetS and OSA, in the present review, we aimed to collate and summarise the potential pathophysiological mechanisms linking these pathologies. In short, obesity appears to promote OSA development via multiple pathways, some of which are not directly related to mass but rather to metabolic complications of obesity. Simultaneously, OSA promotes weight gain through central mechanisms. On the other hand, diabetes mellitus contributes to OSA pathophysiology mainly through effects on peripheral nerves and carotid body desensitization, while intermittent hypoxia and sleep fragmentation are the principal culprits in OSA-mediated diabetes. Apart from a bidirectional pathophysiological relationship, obesity and diabetes mellitus together additively increase cardiovascular risk in OSA patients. Additionally, the emergence of new drugs targeting obesity and unequivocal results of the available studies underscore the need for further exploration of the mechanisms linking MetS and OSA, all with the aim of improving outcomes in these patients.

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