White adipose tissue resilience to insulin deprivation and replacement.

Adipocyte size and body fat distribution are strongly linked to the metabolic complications of obesity. The aim of the present study was to test the plasticity of white adipose tissue in response to insulin deprivation and replacement. We have characterized the changes of adipose cell size repartiti...

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Main Authors: Lilas Hadji, Emmanuelle Berger, Hédi Soula, Hubert Vidal, Alain Géloën
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4149534?pdf=render
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spelling doaj-cb4df3f5cbb34f3e879486b857df03172020-11-25T02:37:10ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0198e10621410.1371/journal.pone.0106214White adipose tissue resilience to insulin deprivation and replacement.Lilas HadjiEmmanuelle BergerHédi SoulaHubert VidalAlain GéloënAdipocyte size and body fat distribution are strongly linked to the metabolic complications of obesity. The aim of the present study was to test the plasticity of white adipose tissue in response to insulin deprivation and replacement. We have characterized the changes of adipose cell size repartition and gene expressions in type 1 diabetes Sprague-Dawley rats and type 1 diabetic supplemented with insulin.Using streptozotocin (STZ)-induced diabetes, we induced rapid changes in rat adipose tissue weights to study the changes in the distribution of adipose cell sizes in retroperitoneal (rWAT), epididymal (eWAT) and subcutaneous adipose tissues (scWAT). Adipose tissue weights of type 1 diabetic rats were then rapidly restored by insulin supplementation. Cell size distributions were analyzed using multisizer IV (Beckman Coulter). Cell size changes were correlated to transcriptional regulation of genes coding for proteins involved in lipid and glucose metabolisms and adipocytokines.The initial body weight of the rats was 465±5.2 g. Insulin privation was stopped when rats lost 100 g which induced reductions in fat mass of 68% for rWAT, 42% for eWAT and 59% for scWAT corresponding to decreased mode cell diameters by 31.1%, 20%, 25.3%, respectively. The most affected size distribution by insulin deprivation was observed in rWAT. The bimodal distribution of adipose cell sizes disappeared in response to insulin deprivation in rWAT and scWAT. The most important observation is that cell size distribution returned close to control values in response to insulin treatment. mRNAs coding for adiponectin, leptin and apelin were more stimulated in scWAT compared to other depots in diabetic plus insulin group.Fat depots have specific responses to insulin deprivation and supplementation. The results show that insulin is a major determinant of bimodal cell repartition in adipose tissues.http://europepmc.org/articles/PMC4149534?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Lilas Hadji
Emmanuelle Berger
Hédi Soula
Hubert Vidal
Alain Géloën
spellingShingle Lilas Hadji
Emmanuelle Berger
Hédi Soula
Hubert Vidal
Alain Géloën
White adipose tissue resilience to insulin deprivation and replacement.
PLoS ONE
author_facet Lilas Hadji
Emmanuelle Berger
Hédi Soula
Hubert Vidal
Alain Géloën
author_sort Lilas Hadji
title White adipose tissue resilience to insulin deprivation and replacement.
title_short White adipose tissue resilience to insulin deprivation and replacement.
title_full White adipose tissue resilience to insulin deprivation and replacement.
title_fullStr White adipose tissue resilience to insulin deprivation and replacement.
title_full_unstemmed White adipose tissue resilience to insulin deprivation and replacement.
title_sort white adipose tissue resilience to insulin deprivation and replacement.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2014-01-01
description Adipocyte size and body fat distribution are strongly linked to the metabolic complications of obesity. The aim of the present study was to test the plasticity of white adipose tissue in response to insulin deprivation and replacement. We have characterized the changes of adipose cell size repartition and gene expressions in type 1 diabetes Sprague-Dawley rats and type 1 diabetic supplemented with insulin.Using streptozotocin (STZ)-induced diabetes, we induced rapid changes in rat adipose tissue weights to study the changes in the distribution of adipose cell sizes in retroperitoneal (rWAT), epididymal (eWAT) and subcutaneous adipose tissues (scWAT). Adipose tissue weights of type 1 diabetic rats were then rapidly restored by insulin supplementation. Cell size distributions were analyzed using multisizer IV (Beckman Coulter). Cell size changes were correlated to transcriptional regulation of genes coding for proteins involved in lipid and glucose metabolisms and adipocytokines.The initial body weight of the rats was 465±5.2 g. Insulin privation was stopped when rats lost 100 g which induced reductions in fat mass of 68% for rWAT, 42% for eWAT and 59% for scWAT corresponding to decreased mode cell diameters by 31.1%, 20%, 25.3%, respectively. The most affected size distribution by insulin deprivation was observed in rWAT. The bimodal distribution of adipose cell sizes disappeared in response to insulin deprivation in rWAT and scWAT. The most important observation is that cell size distribution returned close to control values in response to insulin treatment. mRNAs coding for adiponectin, leptin and apelin were more stimulated in scWAT compared to other depots in diabetic plus insulin group.Fat depots have specific responses to insulin deprivation and supplementation. The results show that insulin is a major determinant of bimodal cell repartition in adipose tissues.
url http://europepmc.org/articles/PMC4149534?pdf=render
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