Few studies have investigated the effect of OSAS on GV measured with a CGM system (Table 1). Using a CGM system, Bialasiewicz et al. [17] investigated whether sleep disordered breathing (SDB) influences interstitial glucose concentrations (IGC) in rapid eye movement (REM) and non-REM (NREM) sleep stage. Among 32 individuals, 11 with periodical SDB were included. Periodical SDB was defined as the presence of a pair of REM or NREM sleep periods on PSG complicated with apnoeas/hypopnoeas and free from apnoeas/hypopnoeas. The AHI for defining the SDB periods was ≥ 10. Measurements of IGC during REM and NREM sleep with and without SDB (REM-no-SDB, NREM-no-SDB and REM-SDB, NREM-SDB, respectively) were obtained [17]. There was a decrease in blood glucose only during REM sleep among individuals without SDB. The mean change in IGC was lower than that of NREM-no-SDB by almost tenfold: −0.047 ± 0.051 versus − 0.005 ± 0.022 mmol/l 5 min(−1), respectively (p = 0.019). However, glucose did not decrease during REM sleep in the case of SDB. More interestingly, in NREM sleep stage, SDB did not significantly affect glucose [17].

Elizur et al. [18] studied the effect of hypoxaemia and nocturnal glucose in seven individuals without DM with moderate-to-severe OSAS. Mean oxygen saturation (SpO2) and percentage of time spent at SpO2 < 90% during sleep were recorded. No consistent correlation between oxygen saturation variables and blood glucose was found. However, using a CGM system, a lower mean SpO2 correlated with decreased GV during REM sleep (r = 0.790, p = 0.034), among individuals with significant desaturation during night sleep (> 30% versus < 10% of the night sleep with SpO2 < 90%) (p = 0.030) in comparison to participants with mild desaturation [18].

Another study [19] investigated blood glucose and GV, using a CGM system, among people with OSAS both in the night during sleep and throughout the day. Eighty-six individuals with OSAS and 40 controls were studied [19]. People with OSAS had significantly higher average daily glucose than those without OSAS (6.31 ± 0.61 versus 4.94 ± 0.78 mg/dl, p < 0.010). Interestingly, both mean glucose and post-prandial glucose peaks were significantly higher and prolonged among individuals with OSAS compared with controls. Furthermore, among people with OSAS, higher blood glucose fluctuation coefficient (BGFC, 1.930 ± 0.710 versus 1.210 ± 0.380 mmol/L, p < 0.050), mean amplitude of glycaemic excursions (MAGE, 4.180 ± 0.650 versus 2.180 ± 0.480 mmol/L, p < 0.050) and night mean amplitude of glycaemic excursions (NMAGE, 2.000 ± 0.530 versus 1.110 ± 0.430 mmol/L, p < 0.050) were observed. Moreover, there was a significant positive correlation of MAGE and NMAGE with insulin resistance index (IRI) and AHI (r = 0.318 and 0.349, respectively) (p < 0.010 or 0.001) [19].

A close correlation between obesity, T2DM and OSAS has been observed [20]. Intermittent hypoxia in OSAS induces oxidative stress and sympathetic nervous activity, which increases blood glucose. Furthermore, a bidirectional relationship between obesity and OSAS has been proposed [21, 22]. Short sleep duration and sleep fragmentation trigger neuroendocrine disorders that increase appetite and food consumption, while untreated OSAS aggravates daytime sleepiness [21]. The latter promotes a sedentary lifestyle, and thus a further increase in weight gain and T2DM [21]. Moreover, obesity is associated with fat deposition in the neck, which increases the possibility of airway collapse during sleep. Finally, abdominal obesity is a risk factor for OSAS through a number of physiological and anatomical mechanisms [21].

Hui et al. [23] investigated the relationship between SpO2 and interstitial glucose (IGL) in 130 patients with both OSAS and T2DM. Participants were divided into three groups, according to the lowest SpO2% (LSpO2%) tested (mild, moderate and severe LSpO2). PSG and CGM systems were used. LSpO2 during sleep stimulated an increase in IGL [23]. Both average nocturnal IGL and peak IGL in the severe LSpO2 group were significantly higher compared with those in the mild and moderate groups. In stepwise multiple regression analysis, BMI, AHI, homeostatic model assessment for insulin resistance (HOMA-IR), average SpO2 and LSpO2 were the major risk factors for altered IGL in the night among people with OSAS and T2DM [23].

In a cross-sectional study [24], severity of OSAS and dysglycaemia was examined. PSG was conducted in 115 people with OSA, 44 with T2DM and 71 without DM, with an AHI ≥ 20/h. CGM was used in 94 individuals [24]. A significant association was observed between HbA1c and sleep parameters, including AHI, NREM AHI, minimum peripheral capillary oxygen saturation (SpO2) and percentage of time spent sleeping with SpO2 levels < 90% [24]. This finding was seen in the entire study population and in individuals without DM, with all p-values < 0.050. However, this association was not noted in individuals with T2DM [24]. Interestingly, mean glucose was significantly higher in participants with severe OSAS compared with those without OSAS (p = 0.048) [24]. More importantly, after adjusting for confounding factors, such as age, sex and BMI, the correlation between mean blood glucose and non-REM AHI remained significant (β = 0.233, p = 0.030) [24]. Additionally, among individuals without DM, there was a significant correlation between mean blood glucose and AHI (r = 0.363, p = 0.004), as well as between mean glucose and non-REM AHI (r = 0.378, p = 0.003), even after accounting for confounding variables [24].

The role of CGM among people with OSAS but without DM was further studied [6]. Dynamic nocturnal glucose changes among 11 individuals with moderate to severe OSAS were compared with those obtained from other 12 individuals with mild or no OSAS [6]. Different trends in nocturnal blood glucose were observed among people with different severity of OSAS. Among participants with moderate-to-severe OSAS, glucose increased after sleep onset, whereas glucose of participants without OSAS or with mild OSAS had a decreasing trend during the first stage of sleep (F = 8.933, p < 0.001) [6]. Moreover, increasing glucose after sleep onset was associated with OSAS features, namely sleep fragmentation, desaturation and autonomic dysfunction [6].

Khaire et al. [12] assessed GV in individuals with T2DM and OSAS and in controls. There were four groups of participants: Group A (20 individuals with DM and OSAS), Group B (20 with DM without OSAS), Group C (10 without DM with OSAS) and Group D (10 without DM or OSAS) [12]. Participants underwent CGM and PSG. The GV parameters night CV, MAGE and NMAGE were significantly higher in Group A compared with Group B (p < 0.050) and significantly higher in Group C compared with Group D (p < 0.050). Moreover, there was a positive correlation of AHI with glucose SD, MAGE and NMAGE in all groups [12].

Another study [25] addressed the question whether CGM-derived metrics in individuals with T2DM differ according to OSAS severity. Among 207 participants with T2DM and OSAS (average age 61 years, 54% male patients, mean HbA1c 7.2%), 50% had a mild OSAS (oxygen desaturation index [ODI] > 5/h) and 50% had a moderate-to-severe OSAS (ODI > 15/h). Median CGM use was 11 days. Participants with moderate-to-severe OSAS had higher mean glucose during sleep (adjusted difference 8.4 mg/dL, p = 0.030) and during wake period (adjusted difference 7.1 mg/dL, p = 0.060) compared with those with mild OSAS [25]. Furthermore, the presence of moderate-to-severe OSAS was associated with lower odds for having blood glucose within time-in-range (TIR) during the wake period compared with mild OSAS (adjusted odds ratio 0.630, p = 0.020). MAGE and standard deviation (SD)-ROC were also higher in moderate-to-severe than in mild OSAS, but these were driven by blood glucose during wake period [25].

Similarly, among 174 people with T2DM, Sergazinov et al. [26] showed that individuals with moderate-to-severe OSAS exhibited higher blood glucose than those with mild OSAS [26].

The presence of OSAS among individuals with T1DM, particularly among those with a long duration of T1DM, appears to be high, but it remains frequently underdiagnosed [7]. It has been proposed that sleep disturbances among people with T1DM have a negative impact on glucose metabolism through decreased insulin sensitivity, similar to those with T2DM, but irrespective of BMI [4]. Moreover, OSAS in people with T1DM has been associated with autonomic or peripheral neuropathy, but the link is yet not clear. It has been suggested that neuropathy affects upper airway reflexes, leading to obstruction [4].

More interestingly, very few studies have assessed the role of CGM in OSAS among people with T1DM (Table 1).

A study conducted of 50 young participants with T1DM, 12–16 years old, who were compared with 40 matched controls, showed that those who had a total AHI ≥ 1.5/h reported higher blood glucose according to CGM metrics (mean glucose 208.5 mg/dL, SD: 44.15 mg/dL) and higher percentage of time spent in high glucose (54.17%, SD: 19.10%) compared with those who had a total-AHI < 1.5 (169.52 mg/dl, SD: 45.84 mg/dL and 36.64%, SD: 22.59%, respectively). Interestingly, HbA1c was similar in both groups [27]. This data provides evidence that even mild SDB contributes to hyperglycaemic episodes in young people with T1DM. Moreover, the percentage of time spent in sleep-stage N2 was positively associated with HbA1c (p < 0.001), average blood glucose on CGM (p = 0.014) and the percentage of time spent in high glucose (p = 0.030) [27].

Kostkova et al. [28] examined sleep in 44 children with T1DM (without chronic complications, obesity/overweight or hypoglycaemia) and 60 controls (10–19 years of age) and how short-term metabolic control could affect sleep quality and SDB. Participants underwent PSG and CGM (for 4 days). There were no significant differences between the two groups in terms of total sleep duration and quality, percentage of sleep stages and respiratory parameters. However, a better short-term glycaemic control (average sensor glucose, AvgSG < 10 mmol/l, N = 18) was associated with significantly lower AHI: 0.3 (0–0.5) versus 0.6 (0.2–0.9) events/h, p < 0.05, compared with suboptimal short-term control (N = 26). The same was seen for respiratory arousal index: 0 (0–0.1) versus 0.2 (0–0.3), p < 0.019. Among participants with T1DM, one was diagnosed with OSAS and nine were diagnosed with mild central apnoea [28].

Basille et al. [29] assessed SDB and GV in T1DM participants in a single-centre study. In total, 46 adults with T1DM (25 men) with median age 42 (35–54) years and mean BMI 24.8 (23.0–28.9) kg/m2 underwent PSG and CGM during a night. Mild and moderate-to-severe SDB were defined as an AHI > 5/h and > 15/h, respectively. There was a high prevalence of SDB (37%). Participants with moderate-to-severe OSAS had a higher BMI and a longer DM duration compared with those with mild SDB or without SDB [29]. Moreover, participants with moderate-to-severe OSAS were not more symptomatic and did not have more GV or hypoglycaemic episodes. Finally, sleep disorders were not associated with above-target GV or with hypoglycaemic episodes [29]. On the basis of these findings, the authors proposed that people with T1DM who have a BMI ≥ 30 kg/m2 should be screened for SDB [29].