title: Reduced gene expression of adiponectin in fat tissue from patients with end-stage renal disease.
abstract: BACKGROUND
  Cardiovascular disease (CVD) is the main cause of death in end-stage renal disease (ESRD) patients. It has been suggested that inflammation plays a key role in the development of both atherosclerosis and malnutrition (MIA), a combination of complications associated with poor outcome. Although plasma levels of adiponectin, a recently discovered anti-inflammatory and antiatherogenic adipocytokine, are markedly elevated in ESRD, gene expression of adiponectin (ApM1) has not been analyzed in ESRD patients.
  
  
  METHODS
  We analyzed the ApM1 gene expression in adipose tissue from 18 ESRD patients of whom 9 (7 males, 60 +/- 8 years, BMI 24 +/- 6 kg/m(2)) had a high prevalence of MIA complications, and 9 age- (55 +/- 9 years), gender- (7 males) and BMI- (24 +/- 2 kg/m(2)) matched ESRD patients had few MIA complications. The results were compared with age- (59 +/- 11 years), gender- (7 males), and BMI- (24 +/- 6 kg/m(2)) matched healthy control patients. Information on CVD was obtained at the recruitment based on a detailed medical history. Malnutrition was defined as a subjective global assessment (SGA) score >1. Inflammation was defined as CRP >/=10 mg/L. Gene expression analysis was performed using the in situ hybridization technique.
  
  
  RESULTS
  Gene expression of ApM1 was lower in ESRD patients compared with healthy control patients (P= 0.001). On the other hand, when comparing the gene expression between ESRD patients with and without MIA complications, respectively, no difference in the ApM1 gene expression was detected.
  
  
  CONCLUSIONS
  Adiponectin gene expression is significantly down-regulated in ESRD patients compared with healthy control patients. We propose that the decrease in expression may be the result of a negative feedback regulation, as a result of elevated levels of circulating adiponectin caused by renal failure.
authors.affiliation: Department of Molecular Medicine, Divisions of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Alicia
authors.initials: A
authors.lastname: Marchlewska
authors.forename: Peter
authors.initials: P
authors.lastname: Stenvinkel
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindholm
authors.forename: Anders
authors.initials: A
authors.lastname: Danielsson
authors.forename: Roberto
authors.initials: R
authors.lastname: Pecoits-Filho
authors.forename: Fredrik
authors.initials: F
authors.lastname: Lönnqvist
authors.forename: Martin
authors.initials: M
authors.lastname: Schalling
authors.forename: Olof
authors.initials: O
authors.lastname: Heimbürger
authors.forename: Louise
authors.initials: L
authors.lastname: Nordfors
mesh_terms: D052242:Adiponectin; D000273:Adipose Tissue / Q000378:metabolism*; D000368:Aged; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000150:complications; D015536:Down-Regulation; D005260:Female; D015870:Gene Expression; D006801:Humans; D007249:Inflammation / Q000150:complications; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000235:genetics / Q000378:metabolism*; D008297:Male; D044342:Malnutrition / Q000150:complications; D008875:Middle Aged
chemical_list: D052242:Adiponectin; D036341:Intercellular Signaling Peptides and Proteins