ANNALS OF THE NEW YORK ACADEMY OF SCIENCES Issue: The Brain and Obesity Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (original) (raw)
Related papers
Interacting epidemics? Sleep curtailment, insulin resistance, and obesity
Annals of the New York Academy of Sciences, 2012
In the last 50 years, the average self-reported sleep duration in the United States has decreased by 1.5-2 hours in parallel with an increasing prevalence of obesity and diabetes. Epidemiological studies and meta-analyses report a strong relationship between short or disturbed sleep, obesity, and abnormalities in glucose metabolism. This relationship is likely to be bidirectional and causal in nature, but many aspects remain to be elucidated. Sleep and the internal circadian clock influence a host of endocrine parameters. Sleep curtailment in humans alters multiple metabolic pathways, leading to more insulin resistance, possibly decreased energy expenditure, increased appetite, and immunological changes. On the other hand, psychological, endocrine, and anatomical abnormalities in individuals with obesity and/or diabetes can interfere with sleep duration and quality, thus creating a vicious cycle. In this review, we address mechanisms linking sleep with metabolism, highlight the need for studies conducted in real-life settings, and explore therapeutic interventions to improve sleep, with a potential beneficial effect on obesity and its comorbidities.
Diabetes, 2015
Recent increases in the prevalence of obesity and type 2 diabetes mellitus (T2DM) in modern societies have been paralleled by reductions in the time their denizens spend asleep. Epidemiological studies have shown that disturbed sleep-comprising short, low-quality, and mistimed sleep-increases the risk of metabolic diseases, especially obesity and T2DM. Supporting a causal role of disturbed sleep, experimental animal and human studies have found that sleep loss can impair metabolic control and body weight regulation. Possible mechanisms for the observed changes comprise sleep loss-induced changes in appetite-signaling hormones (e.g., higher levels of the hunger-promoting hormone ghrelin) or hedonic brain responses, altered responses of peripheral tissues to metabolic signals, and changes in energy intake and expenditure. Even though the overall consensus is that sleep loss leads to metabolic perturbations promoting the development of obesity and T2DM, experimental evidence supporting...
Short sleep duration and obesity: mechanisms and future perspectives
Cell Biochemistry and Function, 2012
A reduction of sleep time has become common over the last century, and growing evidence from both epidemiological and laboratory-based studies suggests sleep curtailment is a new risk factor for the development of obesity. On this basis, the present review examines the role of sleep curtailment in the metabolic and endocrine alterations, including decreased glucose tolerance and insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin and increased hunger and appetite. It will be discussed how sleep restriction may lead to increase in food intake and result in greater fatigue, which may favour decreased energy expenditure. Altogether, evidences point to a possible role of decreased sleep duration in the current epidemic of obesity and therefore present literature highlights the importance of getting enough good sleep for metabolic health. Many aspects still need to be clarified and intervention studies also need to be conducted.
Impact of Sleep and Sleep Loss on Neuroendocrine and Metabolic Function
Hormone Research, 2007
It has been known for several decades that sleep exerts profound modulatory effects on hormones and metabolism. The secretion of growth hormone (GH) and prolactin (PRL) is markedly increased during sleep, whereas the release of cortisol and thyrotropin (TSH) is inhibited. Conversely, awakenings interrupting sleep inhibit nocturnal GH and PRL secretions and are associated with increased cortisol and TSH concentrations. Modulatory effects of sleep on endocrine release are not limited to the hormones of the hypothalamic-pituitary axis. Indeed the hormonal control of carbohydrate metabolism and water and electrolyte balance is also different during total sleep deprivation as compared with normal sleep.
Metabolic effects of sleep disruption, links to obesity and diabetes
Purpose of the review-To highlight the adverse metabolic effects of sleep disruption and to open ground for research aimed at preventive measures. This area of research is especially relevant given the increasing prevalence of voluntary sleep curtailment, sleep disorders, diabetes, and obesity.
Review The metabolic burden of sleep loss
In parallel with the increasing prevalence of obesity and type 2 diabetes, sleep loss has become common in modern societies. An increasing number of epidemiological studies show an association between short sleep duration, sleep disturbances, and circadian desynchronisation of sleep with adverse metabolic traits, in particular obesity and type 2 diabetes. Furthermore, experimental studies point to distinct mechanisms by which insufficient sleep adversely affects metabolic health. Changes in the activity of neuroendocrine systems seem to be major mediators of the detrimental metabolic effects of insufficient sleep, through favouring neurobehavioural outcomes such as increased appetite, enhanced sensitivity to food stimuli, and, ultimately, a surplus in energy intake. The effect of curtailed sleep on physical activity and energy expenditure is less clear, but changes are unlikely to outweigh increases in food intake. Although long-term interventional studies proving a cause and effect association are still scarce, sleep loss seems to be an appealing target for the prevention, and probably treatment, of metabolic disease.
Sleep and obesity: A focus on animal models
Neuroscience & Biobehavioral Reviews, 2012
The rapid rise in obesity prevalence in the modern world parallels a significant reduction in restorative sleep (Agras et al.Wolk et al., 2003). Reduced sleep time and quality increases the risk for obesity, but the underlying mechanisms remain unclear . A majority of the theories linking human sleep disturbances and obesity rely on self-reported sleep. However, studies with objective measurements of sleep/wake parameters suggest a U-shaped relationship between sleep and obesity. Studies in animal models are needed to improve our understanding of the association between sleep disturbances and obesity. Genetic and experimenter-induced models mimicking characteristics of human obesity are now available and these animal models will be useful in understanding whether sleep disturbances determine propensity for obesity, or result from obesity. These models exhibit weight gain profiles consistently different from control animals. Thus a careful evaluation of animal models will provide insight into the relationship between sleep disturbances and obesity in humans.
Short Sleep Duration, Glucose Dysregulation and Hormonal Regulation of Appetite in Men and Women
SLEEP, 2000
Epidemiologic studies report an association between selfreported sleep duration and obesity. 1 In fact, obesity and self-reported sleep duration show inverse trends with obesity prevalence increasing over the past decades and sleep duration decreasing. 2 Moreover, there is increasing evidence from clinical studies showing that reducing sleep leads to greater food intake relative to habitual sleep. 3-6 Data on the role of physical activity and energy expenditure on the relationship between sleep duration and obesity are controversial. We 5 and others 4 have found no effect of reducing sleep on energy expenditure, whereas Schmid et al. 7 found that sleep restriction decreased physical activity and Jung et al. 8 found greater energy expenditure during total sleep deprivation relative to habitual sleep.
Sleep–obesity relation: underlying mechanisms and consequences for treatment
Obesity Reviews, 2017
SummaryShort sleep duration has been associated with obesity in numerous epidemiological studies. However, such association studies cannot establish evidence of causality. Clinical intervention studies, on the other hand, can provide information on a causal effect of sleep duration on markers of weight gain: energy intake and energy expenditure. Herein is an overview of the science related to the impact of sleep restriction, in the context of clinical intervention studies, on energy intake, energy expenditure and body weight. Additionally, studies that evaluate the impact of sleep restriction on weight loss and the impact of sleep extension on appetite are discussed. Information to date suggests that weight management is hindered when attempted in the context of sleep restriction, and the public should be made aware of the negative consequences of sleep restriction for weight regulation.