Mechanisms of effects on sleep disruption on adipocyte/obesity metabolism and relation to other metabolic disease

It is now clear that there is a close two-way interrelationship between healthy adipose tissue function and optimal sleep quality and quantity. For example, poor sleep leads to increased appetite, food intake, and weight gain with adverse metabolic impact, while visceral adiposity increases the risk of poor sleep in the form of sleep apnea. Although visceral adiposity was first recognized as a risk factor for sleep apnea several decades ago, the wide-ranging detrimental impact of sleep apnea, and other types of disturbances of sleep quality or quantity, on adipose tissue metabolism have only more recently been appreciated. Examples include alteration of adipocytokine profiles, promotion of systemic inflammation, and disturbances of lipid metabolism. Such derangements of adipose tissue function in turn result in increased risk of serious metabolic diseases such as diabetes. Inherent challenges in dissection of the molecular mechanisms connecting cues for sleep quality and quantity to adipose tissue function include the circadian nature of sleep cycles and the possible limitations of animal models of sleep disturbance to reflect the human setting.

The editors of AJP - E&M encourage submission of manuscripts reporting on the molecular and physiological mechanisms whereby cues of poor sleep quality or quantity are translated to direct effects on adipose tissue function. These may examine the impact of sleep apnea or other intermittent hypoxia, disrupted REM sleep, altered circadian sleep cycles, or other types of sleep disturbances that have relevance to human metabolic diseases. Areas of particular interest include but are not limited to 1) addressing sex-specific effects, 2) transgenerational impact, 3) novel signaling factors, 4) differential mechanisms of sleep quality or quantity effects across white adipose depots and in brown adipose tissue, 5) role of the gut microbiota. Studies that develop, validate, and utilize additional types of animal models of sleep quality or quantity, or utilize transgenic or null mouse models to gain mechanistic insights, are also encouraged. However, purely descriptive studies reporting on changes in adipocyte gene expression or function in either human or other species, even if comprehensive in nature, are not suitably responsive to this Call. We will consider both original research articles and review articles. For review articles only, authors should email the editorial office (karen.dodson@wustl.edu) with a pre-submission inquiry including a working title, author and affiliation list, abstract, and brief outline of the content for approval by the editors.  

Submission Deadline: September 30, 2017

From: 
Email:  
To: 
Email:  
Subject: 
Message:

~/Custom.Templates/Document.aspx