2.50
Hdl Handle:
http://hdl.handle.net/10755/211709
Type:
Research Study
Title:
ROLE OF SLEEP in THE REGULATION OF APPETITE AND GLUCOSE METABOLISM
Abstract:
Purpose/Background: The prevalence of adolescent obesity has increased worldwide. One modifiable risk factor that has received little attention is quantity of sleep.  Sleep loss has become a common behavior across the lifespan in modern society. Cumulative evidence suggests a dose-response relationship between short sleep duration and high body mass index (BMI) has been reported across all age groups. How sleep loss may interact with body weight is unknown, but the circadian rhythmicity of the hormones regulating appetite and energy expenditure may be involved. A number of hormones may mediate the interactions between short sleep duration, glucose metabolism, and high BMI.  Two key opposing hormones in appetite regulation, leptin and ghrelin, play a significant role in the interaction between short sleep duration and high BMI. Leptin is an adipocyte-derived hormone that suppresses appetite. Ghrelin is predominantly a stomach-derived peptide that stimulates appetite. Other mediators of metabolism that may contribute include adiponectin and insulin. Adiponectin is a novel hormone secreted by adipocytes and is associated with insulin sensitivity. Methods/Results: To substantiate the association between sleep and metabolic processes in adults and children, fasting (to control hormone fluctuations after food ingestion) blood samples are taken in the morning and stored at -80 C until assayed. For children, local anesthetic cream may be applied to the cubital fossa prior to blood draw. Similarly, overnight urinary collection may be a less-invasive option for children. Leptin and insulin are determined using enzyme-linked immunoassays (ELISA). Total ghrelin (which mainly reflects unacylated or inactive ghrelin levels) and adiponectin are measured by radioimmunoassay. To interpret the assay results, standard curves are plotted using software which can perform four-parameter logistic regression models. Coefficients of variability (CV) should be noted for each assay performed. It is important to understand that leptin circulates at levels proportional to body fat or BMI (possible confounding factors). Profiles of homeostatic model assessment (HOMA) levels, an index of insulin resistance directly proportional to the product of fasting insulin-glucose, are measured with higher values suggesting low insulin sensitivity. Previous studies in adults suggest that major neuroendocrine and metabolic alterations associated with sleep loss are upregulation of appetite, with lower leptin and higher ghrelin levels, leading to increased hunger (especially for high carbohydrate foods) and an abnormal disturbance of glucose regulation that involves decreased insulin sensitivity (elevated HOMA levels), possibly mediating weight gain. Implications: Mounting evidence suggests that sleep loss, a behavior that is specific to humans and appears to have become more prevalent during the past few decades, may increase the risk of obesity and type 2 diabetes mellitus (T2DM). Furthermore, the biological mechanisms underlying these adverse effects of sleep loss remain to be identified, especially in children, and are likely to be multifactorial. The measurement of appetite-regulating hormones and glucose metabolism biomarkers are critical for 1) understanding potential mechanisms among sleep loss, obesity, and T2DM, 2) identifying individuals at greatest risk for obesity and metabolic disorders, and 3) designing interventions to provide primary prevention or early intervention for improved sleep and health outcomes.
Keywords:
Adolescent obesity; Sleep quantity
Repository Posting Date:
20-Feb-2012
Date of Publication:
20-Feb-2012
Other Identifiers:
4940
Sponsors:
Western Institute of Nursing

Full metadata record

DC FieldValue Language
dc.typeResearch Studyen_GB
dc.titleROLE OF SLEEP in THE REGULATION OF APPETITE AND GLUCOSE METABOLISMen_GB
dc.identifier.urihttp://hdl.handle.net/10755/211709-
dc.description.abstractPurpose/Background: The prevalence of adolescent obesity has increased worldwide. One modifiable risk factor that has received little attention is quantity of sleep.  Sleep loss has become a common behavior across the lifespan in modern society. Cumulative evidence suggests a dose-response relationship between short sleep duration and high body mass index (BMI) has been reported across all age groups. How sleep loss may interact with body weight is unknown, but the circadian rhythmicity of the hormones regulating appetite and energy expenditure may be involved. A number of hormones may mediate the interactions between short sleep duration, glucose metabolism, and high BMI.  Two key opposing hormones in appetite regulation, leptin and ghrelin, play a significant role in the interaction between short sleep duration and high BMI. Leptin is an adipocyte-derived hormone that suppresses appetite. Ghrelin is predominantly a stomach-derived peptide that stimulates appetite. Other mediators of metabolism that may contribute include adiponectin and insulin. Adiponectin is a novel hormone secreted by adipocytes and is associated with insulin sensitivity. Methods/Results: To substantiate the association between sleep and metabolic processes in adults and children, fasting (to control hormone fluctuations after food ingestion) blood samples are taken in the morning and stored at -80 C until assayed. For children, local anesthetic cream may be applied to the cubital fossa prior to blood draw. Similarly, overnight urinary collection may be a less-invasive option for children. Leptin and insulin are determined using enzyme-linked immunoassays (ELISA). Total ghrelin (which mainly reflects unacylated or inactive ghrelin levels) and adiponectin are measured by radioimmunoassay. To interpret the assay results, standard curves are plotted using software which can perform four-parameter logistic regression models. Coefficients of variability (CV) should be noted for each assay performed. It is important to understand that leptin circulates at levels proportional to body fat or BMI (possible confounding factors). Profiles of homeostatic model assessment (HOMA) levels, an index of insulin resistance directly proportional to the product of fasting insulin-glucose, are measured with higher values suggesting low insulin sensitivity. Previous studies in adults suggest that major neuroendocrine and metabolic alterations associated with sleep loss are upregulation of appetite, with lower leptin and higher ghrelin levels, leading to increased hunger (especially for high carbohydrate foods) and an abnormal disturbance of glucose regulation that involves decreased insulin sensitivity (elevated HOMA levels), possibly mediating weight gain. Implications: Mounting evidence suggests that sleep loss, a behavior that is specific to humans and appears to have become more prevalent during the past few decades, may increase the risk of obesity and type 2 diabetes mellitus (T2DM). Furthermore, the biological mechanisms underlying these adverse effects of sleep loss remain to be identified, especially in children, and are likely to be multifactorial. The measurement of appetite-regulating hormones and glucose metabolism biomarkers are critical for 1) understanding potential mechanisms among sleep loss, obesity, and T2DM, 2) identifying individuals at greatest risk for obesity and metabolic disorders, and 3) designing interventions to provide primary prevention or early intervention for improved sleep and health outcomes.en_GB
dc.subjectAdolescent obesityen_GB
dc.subjectSleep quantityen_GB
dc.date.available2012-02-20T12:09:43Z-
dc.date.issued2012-02-20T12:09:43Z-
dc.date.accessioned2012-02-20T12:09:43Z-
dc.description.sponsorshipWestern Institute of Nursingen_GB
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