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Review
. 2025 Jul;16(7):1202-1216.
doi: 10.1111/jdi.70075. Epub 2025 Jun 1.

Sleep habits in the pathogenesis and management of diabesity

Affiliations
Review

Sleep habits in the pathogenesis and management of diabesity

Cecilie Holm Rasmussen et al. J Diabetes Investig. 2025 Jul.

Abstract

In parallel with the rising global epidemic of obesity and diabetes, termed "diabesity" to underscore the strong relationship between these two conditions, there has been a decreasing trend in the average sleep duration in many parts of the world. Sleep is an essential component of everyday life and plays a pivotal role in regulating energy metabolism and many other physiological functions. Updated guidelines include adequate sleep as one of the key elements of lifestyle therapy in diabetes management. From epidemiological studies, there are many researchers across the globe demonstrating a U-shaped relationship between sleep duration and glycemia, as well as more adverse clinical outcomes (notably cardiovascular events and mortality) with shorter sleep in people with diabetes. Sleep deprivation results in inflammation, neurohormonal dysregulation impacting on appetite control, hedonic pathways, and reward processing and eventually facilitates obesity and diabetes. While there is a wealth of evidence supporting the mechanistic links between short sleep duration, weight gain, and dysglycemia, the reasons why long sleepers have worse metabolic health remain obscure. Not only sleep duration matters, but circadian alignment and quality of sleep are also crucial in optimizing metabolic health. Recognizing the importance of promoting sleep hygiene via non-pharmacological strategies, such as sleep extension interventions and cognitive behavioral therapy, is attracting increasing clinical attention to prevent and manage people with diabesity.

Keywords: Cognitive behavioral therapy; Diabesity; Sleep extension therapy.

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Conflict of interest statement

APSK has received research grants and/or speaker honoraria from Abbott, Astra Zeneca, Bayer, Boehringer Ingelheim, Dexcom, Eli‐Lilly, Kyowa Kirin, Merck Serono, Merck Sharp & Dohme, Nestle, Novo‐Nordisk, Pfizer, Sanofi, and Zuellig Pharma. Other authors declared no conflict of interest associated with the contents of this manuscript.

Approval of the research protocol: N/A.

Informed consent: N/A.

Registry and the registration no. of the study/trial: N/A.

Animal studies: N/A.

Figures

Figure 1
Figure 1
The links between abnormal sleep, diabesity and adverse outcomes. While optimal sleep duration for most adults appears to be 6–8 h according to the results of large‐scale epidemiological studies, sleep deprivation and abnormally extended sleep duration exert negative influences on energy and glucose homeostasis resulting in diabesity with increased risk of cardiovascular events and premature death. Abnormal sleep includes not only sleep duration, but also the regularity of sleep habits and sleep quality. Circadian disruptions due to shift work, travelling across time zones and eating late at night have also been shown to increase the risk of obesity, diabetes and metabolic syndrome, eventually leading to cardiovascular events and mortality. People with sleep disorders such as insomnia and obstructive sleep apnoea also have higher risk of diabesity and reduced lifespan than those without these common sleep disorders. Dotted line, possible link pending further evidence from clinical trials; solid line, link supported by evidence from epidemiological and clinical studies.
Figure 2
Figure 2
Possible causal mechanisms between insufficient sleep and diabesity. Insufficient sleep increases the risk of diabesity through its negative effects on insulin sensitivity, pro‐inflammation and possibly appetite regulation. Dotted line, possible link; ↓, decrease; ↑, increase; ↔, no change.

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