title: Relations of adipose tissue CIDEA gene expression to basal metabolic rate, energy restriction, and obesity: population-based and dietary intervention studies.
abstract: BACKGROUND
  Cell death-inducing DNA fragmentation factor-alpha-like effector A (CIDEA) could be a potential target for the treatment of obesity via the modulation of metabolic rate, based on the findings that CIDEA inhibits the brown adipose tissue uncoupling process in rodents.
  
  
  OBJECTIVE
  Our objects were to investigate the putative link between CIDEA and basal metabolic rate in humans and to elucidate further the role of CIDEA in human obesity.
  
  
  METHODS
  We have explored CIDEA gene expression in adipose tissue in two different human studies: a cross-sectional and population-based study assessing body composition and metabolic rate (Mölndal Metabolic study, n = 92); and a longitudinal intervention study of obese subjects treated with a very low calorie diet (VLCD) (VLCD study, n = 24).
  
  
  RESULTS
  The CIDEA gene was predominantly expressed in adipocytes as compared with other human tissues. CIDEA gene expression in adipose tissue was inversely associated with basal metabolic rate independently of body composition, age, and gender (P = 0.014). The VLCD induced an increase in adipose tissue CIDEA expression (P < 0.0001) with a subsequent decrease in response to refeeding (P < 0.0001). Reduced CIDEA gene expression was associated with a high body fat content (P < 0.0001) and high insulin levels (P < 0.01). No dysregulation of CIDEA expression was observed in individuals with the metabolic syndrome when compared with body mass index-matched controls. In a separate sample of VLCD-treated subjects (n = 10), uncoupling protein 1 expression was reduced during diet (P = 0.0026) and inversely associated with CIDEA expression (P = 0.0014).
  
  
  CONCLUSIONS
  The findings are consistent with the concept that CIDEA plays a role in adipose tissue energy expenditure.
authors: Department of Molecular and Clinical Medicine and Wallenberg Laboratory for Cardiovascular Research, Institute of Medicine, the Sahlgrenska Academy, Göteborg University, SE-413 45 Göteborg, Sweden anders.gummesson@gu.se
authors: Anders
authors: A
authors: Gummesson
authors: Margareta
authors: M
authors: Jernås
authors: Per-Arne
authors: PA
authors: Svensson
authors: Ingrid
authors: I
authors: Larsson
authors: Camilla A M
authors: CA
authors: Glad
authors: Erik
authors: E
authors: Schéle
authors: Lena
authors: L
authors: Gripeteg
authors: Kajsa
authors: K
authors: Sjöholm
authors: Theodore C
authors: TC
authors: Lystig
authors: Lars
authors: L
authors: Sjöström
authors: Björn
authors: B
authors: Carlsson
authors: Björn
authors: B
authors: Fagerberg
authors: Lena M S
authors: LM
authors: Carlsson
mesh_terms: D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000375:Aging / Q000502:physiology; D000886:Anthropometry; D051017:Apoptosis Regulatory Proteins / Q000235:genetics*; D001823:Body Composition / Q000502:physiology; D031204:Caloric Restriction; D003430:Cross-Sectional Studies; D005260:Female; D015870:Gene Expression / Q000235:genetics / Q000502:physiology; D006801:Humans; D007473:Ion Channels / Q000096:biosynthesis / Q000235:genetics; D008137:Longitudinal Studies; D008297:Male; D024821:Metabolic Syndrome / Q000235:genetics; D008660:Metabolism / Q000502:physiology; D008875:Middle Aged; D024101:Mitochondrial Proteins / Q000096:biosynthesis / Q000235:genetics; D009765:Obesity / Q000178:diet therapy / Q000235:genetics* / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D011153:Population; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012727:Sex Characteristics; D000071256:Uncoupling Protein 1
chemical_list: D051017:Apoptosis Regulatory Proteins; C502539:CIDEA protein, human; D007473:Ion Channels; D024101:Mitochondrial Proteins; C000604371:UCP1 protein, human; D000071256:Uncoupling Protein 1; D012313:RNA