Sleep influences on obesity, insulin resistance, and risk of type 2 diabetes

Highlights

• Experimental sleep restriction led to changes in appetite regulating hormones and increased hunger.

• Caloric intake often exceeded slight increase in energy expenditure, leading to positive energy balance and weight gain.

• Sleep restriction led to increased insulin resistance and elevated diabetes risk, through multiple mechanistic pathways.

• Multiple pathways are involved in alterations of glucose metabolism.

• Limited available data suggested that sleep fragmentation led to alterations in glucose metabolism.

• Behavioral sleep extension and sleep quality improvement may help reduce obesity and diabetes risk.

Abstract

A large body of epidemiologic evidence has linked insufficient sleep duration and quality to the risk of obesity, insulin resistance and type 2 diabetes. To address putative causal mechanisms, this review focuses on laboratory interventions involving several nights of experimental sleep restriction, fragmentation or extension and examining metabolically relevant outcomes. Sleep restriction has been consistently shown to increase hunger, appetite and food intake, with the increase in caloric intake in excess of the energy requirements of extended wakefulness. Findings regarding decreases in hormones promoting satiety or increases in hormones promoting hunger have been less consistent, possibly because of confounding effects of changes in adiposity when energy intake was not controlled and sampling protocols that did not cover the entire 24-h cycle. Imaging studies revealed alterations in neuronal activity of brain regions involved in food reward. An adverse impact of experimental sleep restriction on insulin resistance, leading to reduced glucose tolerance and increased diabetes risk, has been well-documented. There is limited evidence indicating that sleep fragmentation without reduction in sleep duration also results in a reduction in insulin sensitivity. The adverse metabolic outcomes of sleep disturbances appear to involve multiple mechanistic pathways acting in concert. Emerging evidence supports the benefits of behavioral, but not pharmacological, sleep extension on appetite and glucose metabolism. Further research should focus on the feasibility and efficacy of strategies to optimize sleep duration and quality on obesity and diabetes risk in at-risk populations as well as those with established diseases. Further work is needed to identify mechanistic pathways.

Introduction

Approximately one third of human's lifetime is spent sleeping. Sleep is a state of energy restoration and replenishment. In modern society, bedtime is often curtailed to meet increasing personal and social demands. In the United States, self-reported sleep duration has declined over the last 2–3 decades [1]. The epidemics of obesity and diabetes developed simultaneously. Evidence from large cross sectional and longitudinal epidemiologic studies, discussed elsewhere in detail in other articles in this series, demonstrated that insufficient sleep is a risk factor for obesity and diabetes [2,3]. Moreover, poor sleep quality has been linked to similar detrimental effects [3]. To elucidate potential causal mechanisms, this review will focus on the findings from laboratory studies involving the impact of experimental sleep manipulations, including sleep restriction, fragmentation and sleep extension on the control of energy balance and/or glucose metabolism.