title: Primary hyperparathyroidism influences the expression of inflammatory and metabolic genes in adipose tissue.
abstract: BACKGROUND
  Primary hyperparathyroidism (PHPT) is characterised by increased production of parathyroid hormone (PTH) resulting in elevated serum calcium levels. The influence on bone metabolism with altered bone resorption is the most studied clinical condition in PHPT. In addition to this, patients with PHPT are at increased risk of non-skeletal diseases, such as impaired insulin sensitivity, arterial hypertension and increased risk of death by cardiovascular diseases (CVD), possibly mediated by a chronic low-grade inflammation. The aim of this study was to investigate whether adipose tissue reflects the low-grade inflammation observed in PHPT patients.
  
  
  RESULTS
  Subcutaneous fat tissue from the neck was sampled from 16 non-obese patients with PHPT and from 16 patients operated for benign thyroid diseases, serving as weight-matched controls. RNA was extracted and global gene expression was analysed with Illumina BeadArray Technology. We found 608 differentially expressed genes (q-value<0.05), of which 347 were up-regulated and 261 were down-regulated. Gene ontology analysis showed that PHPT patients expressed increased levels of genes involved in immunity and defense (e.g. matrix metallopeptidase 9, S100 calcium binding protein A8 and A9, CD14, folate receptor 2), and reduced levels of genes involved in metabolic processes. Analysis of transcription factor binding sites present in the differentially expressed genes corroborated the up-regulation of inflammatory processes.
  
  
  CONCLUSIONS
  Our findings demonstrate that PHPT strongly influences gene regulation in fat tissue, which may result in altered adipose tissue function and release of pathogenic factors that increase the risk of CVD.
authors.affiliation: Institute of Medicine, University of Bergen, Bergen, Norway.
authors.forename: Monika H E
authors.initials: MH
authors.lastname: Christensen
authors.forename: Simon N
authors.initials: SN
authors.lastname: Dankel
authors.forename: Yngve
authors.initials: Y
authors.lastname: Nordbø
authors.forename: Jan Erik
authors.initials: JE
authors.lastname: Varhaug
authors.forename: Bjørg
authors.initials: B
authors.lastname: Almås
authors.forename: Ernst A
authors.initials: EA
authors.lastname: Lien
authors.forename: Gunnar
authors.initials: G
authors.lastname: Mellgren
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D001483:Base Sequence; D016022:Case-Control Studies; D017931:DNA Primers; D004734:Energy Metabolism / Q000235:genetics*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D049950:Hyperparathyroidism, Primary / Q000235:genetics*; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D020411:Oligonucleotide Array Sequence Analysis; D016133:Polymerase Chain Reaction
chemical_list: D017931:DNA Primers; D018836:Inflammation Mediators