title: White adipose tissue resilience to insulin deprivation and replacement.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Université de Lyon, CARMEN INSERM U1060, INSA-Lyon, F-69621, Villeurbanne, France.
authors.forename: Lilas
authors.initials: L
authors.lastname: Hadji
authors.affiliation: Université de Lyon, CARMEN INSERM U1060, INSA-Lyon, F-69621, Villeurbanne, France.
authors.forename: Emmanuelle
authors.initials: E
authors.lastname: Berger
authors.affiliation: Université de Lyon, CARMEN INSERM U1060, INSA-Lyon, F-69621, Villeurbanne, France; IXXI Complex Systems Institute, F-69007, Lyon, France; EPI BEAGLE INRIA F-69621, Villeurbanne, France.
authors.forename: Hédi
authors.initials: H
authors.lastname: Soula
authors.affiliation: Université de Lyon, CARMEN INSERM U1060, INSA-Lyon, F-69621, Villeurbanne, France.
authors.forename: Hubert
authors.initials: H
authors.lastname: Vidal
authors.affiliation: Université de Lyon, CARMEN INSERM U1060, INSA-Lyon, F-69621, Villeurbanne, France.
authors.forename: Alain
authors.initials: A
authors.lastname: Géloën
mesh_terms: D017667:Adipocytes / Q000378:metabolism* / Q000473:pathology; D052436:Adipose Tissue, White; D000818:Animals; D048429:Cell Size; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000172:deficiency / Q000494:pharmacology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D014158:Transcription, Genetic / Q000187:drug effects*
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin