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Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats

As it is a common observation that obesity tends to occur after discontinuation of exercise, we investigated how white adipocytes isolated from the periepididymal fat of animals with interrupted physical training transport and oxidize glucose, and whether these adaptations support the weight regain...

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Autores principales: Sertié, R.A.L., Andreotti, S., Proença, A.R.G., Campaña, A.B., Lima, F.B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Associação Brasileira de Divulgação Científica 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4512105/
https://www.ncbi.nlm.nih.gov/pubmed/26017340
http://dx.doi.org/10.1590/1414-431X20154356
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author Sertié, R.A.L.
Andreotti, S.
Proença, A.R.G.
Campaña, A.B.
Lima, F.B.
author_facet Sertié, R.A.L.
Andreotti, S.
Proença, A.R.G.
Campaña, A.B.
Lima, F.B.
author_sort Sertié, R.A.L.
collection PubMed
description As it is a common observation that obesity tends to occur after discontinuation of exercise, we investigated how white adipocytes isolated from the periepididymal fat of animals with interrupted physical training transport and oxidize glucose, and whether these adaptations support the weight regain seen after 4 weeks of physical detraining. Male Wistar rats (45 days old, weighing 200 g) were divided into two groups (n=10): group D (detrained), trained for 8 weeks and detrained for 4 weeks; and group S (sedentary). The physical exercise was carried out on a treadmill for 60 min/day, 5 days/week for 8 weeks, at 50-60% of the maximum running capacity. After the training protocol, adipocytes isolated from the periepididymal adipose tissue were submitted to glucose uptake and oxidation tests. Adipocytes from detrained animals increased their glucose uptake capacity by 18.5% compared with those from sedentary animals (P<0.05). The same cells also showed a greater glucose oxidation capacity in response to insulin stimulation (34.55%) compared with those from the S group (P<0.05). We hypothesize that, owing to the more intense glucose entrance into adipose cells from detrained rats, more substrate became available for triacylglycerol synthesis. Furthermore, this increased glucose oxidation rate allowed an increase in energy supply for triacylglycerol synthesis. Thus, physical detraining might play a role as a possible obesogenic factor for increasing glucose uptake and oxidation by adipocytes.
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spelling pubmed-45121052015-08-13 Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats Sertié, R.A.L. Andreotti, S. Proença, A.R.G. Campaña, A.B. Lima, F.B. Braz J Med Biol Res Biomedical Sciences As it is a common observation that obesity tends to occur after discontinuation of exercise, we investigated how white adipocytes isolated from the periepididymal fat of animals with interrupted physical training transport and oxidize glucose, and whether these adaptations support the weight regain seen after 4 weeks of physical detraining. Male Wistar rats (45 days old, weighing 200 g) were divided into two groups (n=10): group D (detrained), trained for 8 weeks and detrained for 4 weeks; and group S (sedentary). The physical exercise was carried out on a treadmill for 60 min/day, 5 days/week for 8 weeks, at 50-60% of the maximum running capacity. After the training protocol, adipocytes isolated from the periepididymal adipose tissue were submitted to glucose uptake and oxidation tests. Adipocytes from detrained animals increased their glucose uptake capacity by 18.5% compared with those from sedentary animals (P<0.05). The same cells also showed a greater glucose oxidation capacity in response to insulin stimulation (34.55%) compared with those from the S group (P<0.05). We hypothesize that, owing to the more intense glucose entrance into adipose cells from detrained rats, more substrate became available for triacylglycerol synthesis. Furthermore, this increased glucose oxidation rate allowed an increase in energy supply for triacylglycerol synthesis. Thus, physical detraining might play a role as a possible obesogenic factor for increasing glucose uptake and oxidation by adipocytes. Associação Brasileira de Divulgação Científica 2015-05-26 /pmc/articles/PMC4512105/ /pubmed/26017340 http://dx.doi.org/10.1590/1414-431X20154356 Text en http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Biomedical Sciences
Sertié, R.A.L.
Andreotti, S.
Proença, A.R.G.
Campaña, A.B.
Lima, F.B.
Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats
title Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats
title_full Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats
title_fullStr Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats
title_full_unstemmed Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats
title_short Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats
title_sort fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats
topic Biomedical Sciences
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4512105/
https://www.ncbi.nlm.nih.gov/pubmed/26017340
http://dx.doi.org/10.1590/1414-431X20154356
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