title: Adiponectin expression and metabolic markers in obesity and Type 2 diabetes.
abstract: BACKGROUND
  Adiponectin has emerged over the last decade as a key adipokine linking obesity, insulin resistance, and Type 2 diabetes. However, the molecular mechanisms controlling adiponectin expression in adipose tissue are not fully elucidated. Furthermore, increasing evidence indicates that peroxisome proliferator-activated receptor- γ (PPAR-γ) plays an important, and beneficial, role in modulating adiponectin expression.
  
  
  OBJECTIVE
  The aim of the present study was to assess the separate role of obesity and Type 2 diabetes in the relationship between endogenous PPAR-γ signaling and adiponectin expression in subcutaneous adipose tissue.
  
  
  METHODS
  Enzyme-linked immuno sor bent assay and real time quantitative PCR analysis were carried out in overweight, obese, and/or diabetic Tunisian patients who underwent an abdominal surgery.
  
  
  RESULTS
  These results collectively indicate that circulating levels of adiponectin were decreased in all overweight, obese, and/or diabetic (p<0.001). However, the subcutaneous mRNA expression of adiponectin was reduced only in diabetics (p<0.01) but presents some discrepancies in obese individuals. Moreover, mRNA levels of adiponectin were positively correlated with levels of mRNA encoding PPARγ and its heterodimeric partner retinoid X receptor-α (RXR-α), in both obese and diabetic patients.
  
  
  CONCLUSIONS
  Our study on Tunisian patients shows impaired regulation of circulating and mRNA adiponectin levels dependent of metabolic disorders in obesity and Type 2 diabetes. The data suggest that subcutaneous adipose tissue may play an important role in modulating adiponectin expression in diabetes and obesity. Moreover, adiponectin mRNA could be potentially regulated by endogenous PPARγ/RXRα-dependent pathways.
authors.affiliation: Laboratory of Genetics, Immunology and Human Pathology, Biology Department, Faculté Des Sciences de Tunis, CAMPUS, El Manar University, Tunisia.
authors.forename: S
authors.initials: S
authors.lastname: Kouidhi
authors.forename: S
authors.initials: S
authors.lastname: Jarboui
authors.forename: R
authors.initials: R
authors.lastname: Marrakchi
authors.forename: M-S Clerget
authors.initials: MS
authors.lastname: Froidevaux
authors.forename: I
authors.initials: I
authors.lastname: Seugnet
authors.forename: H
authors.initials: H
authors.lastname: Abid
authors.forename: F
authors.initials: F
authors.lastname: Bchir
authors.forename: M
authors.initials: M
authors.lastname: Brahem
authors.forename: B
authors.initials: B
authors.lastname: Demeneix
authors.forename: H
authors.initials: H
authors.lastname: Guissouma
authors.forename: A Benammar
authors.initials: AB
authors.lastname: Elgaaied
mesh_terms: D052242:Adiponectin / Q000097:blood* / Q000235:genetics; D000273:Adipose Tissue / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D004734:Energy Metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism*; D047495:PPAR gamma / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D047495:PPAR gamma; D012333:RNA, Messenger