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Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss

Insufficient sleep is associated with changes in glucose tolerance, insulin secretion, and insulin action. Despite widespread use of weight-loss diets for metabolic risk reduction, the effects of insufficient sleep on glucose regulation in overweight dieters are not known. To examine the consequence...

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Autores principales: Nedeltcheva, A. V., Imperial, J. G., Penev, P. D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384766/
https://www.ncbi.nlm.nih.gov/pubmed/22513492
http://dx.doi.org/10.1038/oby.2012.97
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author Nedeltcheva, A. V.
Imperial, J. G.
Penev, P. D.
author_facet Nedeltcheva, A. V.
Imperial, J. G.
Penev, P. D.
author_sort Nedeltcheva, A. V.
collection PubMed
description Insufficient sleep is associated with changes in glucose tolerance, insulin secretion, and insulin action. Despite widespread use of weight-loss diets for metabolic risk reduction, the effects of insufficient sleep on glucose regulation in overweight dieters are not known. To examine the consequences of recurrent sleep restriction on 24-hour blood glucose control during diet-induced weight loss, 10 overweight and obese adults (3F/7M; mean [SD] age 41 [5] y; BMI 27.4 [2.0] kg/m(2)) completed two 14-day treatments with hypocaloric diet and 8.5 or 5.5-h nighttime sleep opportunity in random order 7 [3] months apart. Oral and intravenous glucose tolerance test (IVGTT) data, fasting lipids and free-fatty acids (FFA), and 24-hour blood glucose, insulin, C-peptide, and counter-regulatory hormone measurements were collected after each treatment. Participants had comparable weight loss (1.0 [0.3] BMI units) during each treatment. Bedtime restriction reduced sleep by 131 [30] min/day. Recurrent sleep curtailment decreased 24-hour serum insulin concentrations (i.e. enhanced 24-hour insulin economy) without changes in oral glucose tolerance and 24-hour glucose control. This was accompanied by a decline in fasting blood glucose, increased fasting FFA which suppressed normally following glucose ingestion, and lower total and LDL cholesterol concentrations. Sleep-loss-related changes in counter-regulatory hormone secretion during the IVGTT limited the utility of the test in this study. In conclusion, sleep restriction enhanced 24-hour insulin economy without compromising glucose homeostasis in overweight individuals placed on a balanced hypocaloric diet. The changes in fasting blood glucose, insulin, lipid and FFA concentrations in sleep-restricted dieters resembled the pattern of human metabolic adaptation to reduced carbohydrate availability.
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spelling pubmed-33847662013-01-01 Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss Nedeltcheva, A. V. Imperial, J. G. Penev, P. D. Obesity (Silver Spring) Article Insufficient sleep is associated with changes in glucose tolerance, insulin secretion, and insulin action. Despite widespread use of weight-loss diets for metabolic risk reduction, the effects of insufficient sleep on glucose regulation in overweight dieters are not known. To examine the consequences of recurrent sleep restriction on 24-hour blood glucose control during diet-induced weight loss, 10 overweight and obese adults (3F/7M; mean [SD] age 41 [5] y; BMI 27.4 [2.0] kg/m(2)) completed two 14-day treatments with hypocaloric diet and 8.5 or 5.5-h nighttime sleep opportunity in random order 7 [3] months apart. Oral and intravenous glucose tolerance test (IVGTT) data, fasting lipids and free-fatty acids (FFA), and 24-hour blood glucose, insulin, C-peptide, and counter-regulatory hormone measurements were collected after each treatment. Participants had comparable weight loss (1.0 [0.3] BMI units) during each treatment. Bedtime restriction reduced sleep by 131 [30] min/day. Recurrent sleep curtailment decreased 24-hour serum insulin concentrations (i.e. enhanced 24-hour insulin economy) without changes in oral glucose tolerance and 24-hour glucose control. This was accompanied by a decline in fasting blood glucose, increased fasting FFA which suppressed normally following glucose ingestion, and lower total and LDL cholesterol concentrations. Sleep-loss-related changes in counter-regulatory hormone secretion during the IVGTT limited the utility of the test in this study. In conclusion, sleep restriction enhanced 24-hour insulin economy without compromising glucose homeostasis in overweight individuals placed on a balanced hypocaloric diet. The changes in fasting blood glucose, insulin, lipid and FFA concentrations in sleep-restricted dieters resembled the pattern of human metabolic adaptation to reduced carbohydrate availability. 2012-04-19 2012-07 /pmc/articles/PMC3384766/ /pubmed/22513492 http://dx.doi.org/10.1038/oby.2012.97 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Nedeltcheva, A. V.
Imperial, J. G.
Penev, P. D.
Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss
title Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss
title_full Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss
title_fullStr Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss
title_full_unstemmed Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss
title_short Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss
title_sort effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384766/
https://www.ncbi.nlm.nih.gov/pubmed/22513492
http://dx.doi.org/10.1038/oby.2012.97
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