Abstract

Epidemiological studies have shown an association between short or disrupted sleep and an increased risk for metabolic disorders. To assess a possible causal relationship, we examined the effects of experimental sleep disturbance on glucose regulation in Wistar rats under controlled laboratory conditions. Three groups of animals were used: a sleep restriction group (RS), a group subjected to moderate sleep disturbance without restriction of sleep time (DS), and a home cage control group. To establish changes in glucose regulation, animals were subjected to intravenous glucose tolerance tests (IVGTTs) before and after 1 or 8 days of sleep restriction or disturbance. Data show that both RS and DS reduce body weight without affecting food intake and also lead to hyperglycemia and decreased insulin levels during an IVGTT. Acute sleep disturbance also caused hyperglycemia during an IVGTT, yet, without affecting the insulin response. In conclusion, both moderate and severe disturbances of sleep markedly affect glucose homeostasis and body weight control.

Highlights

  • Sleep and metabolism seem to be related

  • There were neither differences in food intake between the

  • This study shows that eight days of sleep disturbance markedly interferes with body weight maintenance and glucose metabolism in rats

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Summary

Introduction

Epidemiological studies have established a link between disturbed sleep and increased risk for the development of obesity and type 2 diabetes [1,2,3,4]. These studies revealed that habitual short sleep is a risk factor, independent of classical risk factors such as BMI, food intake, and reduced exercise. Whether or not these relationships are causal is still a matter of debate [8] Experimental studies in both humans and animals have shown clear effects of sleep deprivation on body temperature, food intake, body weight gain, and energy expenditure [9,10,11,12]. A number of recent experimental studies suggest that even mild sleep disturbance leads to glucose intolerance, the first step in the development of type 2 Diabetes [14, 15]

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