Table 4. Summary of data extracted from articles.

CRP, C-reactive protein; SAA, serum amyloid A; PSD, partial sleep deprivation; CPIR, cephalic phase insulin release; RCT, randomized controlled trial; AI/ANs, American Indians/Alaska Natives; OSA, obstructive sleep apnea; GLP-1, glucagon-like peptide 1; NEFA, non-esterified fatty acid

Author and Year of Publication	Purpose of Study	Number of Patients	Type of Study	Result	Conclusion
Iyegha et al., 2019 [9]	They explored the association between glucose metabolism and sleep quality among people with prediabetes and the possible mechanisms linking poor sleep to glucose intolerance.	155	Observational	Compared to those in the standard glucose group, more people with prediabetes suffered from poor sleep quality. The CRP levels were elevated in the prediabetes group compared to the standard glucose group. A positive correlation was also found between disturbed sleep and CRP.	Poor sleep quality is associated with prediabetes. Increased levels of CRP may be a likely cause underlying the association between poor sleep and prediabetes.
de Oliveira et al., 2017 [10]	They investigated whether SAA production during sleep restrictions contributes to the development of associated comorbidities related to sleep loss.	Six mice, 30 humans	Animal	SAA and endotoxin production was increased to approximately four times normal in case of sleep restriction.	Sleep deprivation precipitates SAA production in healthy mice and humans. Elevated levels of SAA may be a part of the signaling cascade connecting sleep loss to its associated ill-health effects such as obesity and type 2 diabetes.
Cedernaes et al., 2016 [12]	This study investigated the effect of a single night of PSD on fasting insulin sensitivity and CPIR in humans.	16	RCT	PSD was significantly associated with higher peripheral insulin resistance than a night of complete sleep.	This study evidenced that sleeping at least seven hours per night may decrease the risk of developing insulin resistance. They also suggest that an altered CPIR (and subsequent disrupted autonomic signaling, which regulates the CPIR) is probably not likely to be the mechanism through which one night of PSD causes metabolic abnormalities.
So-ngern et al., 2019 [13]	This study explored if extending sleep duration for two weeks would improve glucose tolerance in habitually sleep-deprived individuals.	21	RCT	No significant effects of extending sleep duration were found on any metabolic outcomes.	Glucose tolerance improved only in those individuals who could objectively increase their sleep duration to more than six hours per night. Their findings suggested that a necessary amount of sleep is required to improve metabolism.
Nuyujukian et al., 2016 [14]	This study examined the relationship between self-reported sleep duration and the incidence of type 2 diabetes in a population sample of AI/ANs with prediabetes.	1,899	Observational	The incidence of diabetes was higher among short sleepers (≤ six hours per night) than those sleeping seven hours.	Short sleep duration was significantly associated with increased diabetes risk and reduced weight loss.
Bowman et al., 2019 [15]	This study examined the prospective association between polysomnography and self-reported sleep deprivation with metabolic syndrome.	145	Observational	None of the objectively or subjectively assessed sleep indices were associated with metabolic syndrome.	Cross-sectional associations among objectively and subjectively assessed sleep with metabolic syndrome were insignificant.
Wang et al., 2017 [16]	This study aimed to identify if metabolic syndrome was associated with insomnia.	8,017	Observational	Insomnia was not significantly associated with dysglycemia.	The association between insomnia and dysglycemia was not significant. However, those who had insomnia were more susceptible to increased severity of metabolic abnormalities.
Reutrakul et al., 2017 [17]	This study scrutinized the relationship between sleep quality, duration, OSA, and GLP-1 regulation in participants with abnormal glucose tolerance.	71	Observational	GLP-1 did not vary among those sleeping ≤ 5.75 hours, > 5.75 to < 6.5 hours, or ≥ 6.5 hours per night.	OSA severity, but not habitual sleep duration or quality, was associated with lower GLP-1 response to glucose challenge in patients with abnormal glucose tolerance.
Ness et al., 2019 [18]	This study investigated whether sleep restriction affected NEFA suppression and whether recovery sleep for two nights is enough to rehabilitate metabolic health.	15	RCT	Sleep restriction significantly suppressed NEFA rebound levels. NEFA levels returned to baseline after recovery sleep.	NEFA metabolism was significantly affected by sleep restriction. This study demonstrated that two nights of recovery sleep is insufficient to improve glucose metabolism.
Qian et al., 2018 [19]	This study explored the different effects of the circadian system and circadian misalignment on insulin sensitivity and beta-cell function.	14	RCT	The results demonstrated that the inherent biological circadian system and circadian misalignment affect insulin sensitivity via independent processes.	The biological circadian system reduced glucose sensitivity in the biological evening in comparison to the biological morning by affecting beta-cell function. Circadian misalignment did not affect beta-cell function but reduced glucose tolerance by reducing insulin sensitivity.