title: Serum concentrations and expressions of serum amyloid A and leptin in adipose tissue are interrelated: the Genobin Study.
abstract: OBJECTIVE
  Serum amyloid A (SAA) is a novel link between increased adipose tissue mass and low-grade inflammation in obesity. Little is known about the factors regulating its serum concentration and mRNA levels. We investigated the association between SAA and leptin in obese and normal weight subjects and analyzed the effect of weight reduction on serum SAA concentration and gene expression in adipose tissue of the obese subjects.
  
  
  METHODS
  Seventy-five obese subjects (60+/-7 years, body mass index (BMI) 32.9+/-2.8 kg/m(2), mean+/-s.d.) with impaired fasting plasma glucose or impaired glucose tolerance and other features of metabolic syndrome, and 11 normal weight control subjects (48+/-9 years, BMI 23.7+/-1.9 kg/m(2)) were studied at the baseline. Twenty-eight obese subjects underwent a 12-week intensive weight reduction program followed by 5 months of weight maintenance. Blood samples and abdominal s.c. adipose tissue biopsies were taken at the baseline and after the follow-up. Gene expression was studied using real-time quantitative PCR.
  
  
  RESULTS
  The gene expressions in women and serum concentrations of leptin and SAA were interrelated independently of body fat mass in the obese subjects (r=0.54, P=0.001; r=0.24, P=0.039 respectively). In multiple linear regression analyses, leptin mRNA explained 38% of the variance in SAA mRNA (P=0.002) in the obese women. Weight loss of at least 5% increased SAA mRNA expression by 48 and 36% in men and women, but serum SAA concentrations did not change.
  
  
  CONCLUSIONS
  The association between SAA and leptin suggests an interaction between these two adipokines, which may have implications in inflammatory processes related to obesity and the metabolic syndrome.
authors.affiliation: Department of Clinical Nutrition and Food and Health Research Center, University of Kuopio, PO Box 1627, FIN-70211 Kuopio, Finland. tiina.lappalainen@uku.fi
authors.forename: T
authors.initials: T
authors.lastname: Lappalainen
authors.forename: M
authors.initials: M
authors.lastname: Kolehmainen
authors.forename: U
authors.initials: U
authors.lastname: Schwab
authors.forename: L
authors.initials: L
authors.lastname: Pulkkinen
authors.forename: D E
authors.initials: DE
authors.lastname: Laaksonen
authors.forename: R
authors.initials: R
authors.lastname: Rauramaa
authors.forename: M
authors.initials: M
authors.lastname: Uusitupa
authors.forename: H
authors.initials: H
authors.lastname: Gylling
mesh_terms: D017667:Adipocytes / Q000473:pathology / Q000502:physiology; D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology; D000368:Aged; D001835:Body Weight; D005260:Female; D015870:Gene Expression / Q000502:physiology; D018149:Glucose Intolerance / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D020738:Leptin / Q000235:genetics / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000276:immunology / Q000378:metabolism; D008875:Middle Aged; D009765:Obesity / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D000685:Serum Amyloid A Protein / Q000235:genetics / Q000378:metabolism*; D015431:Weight Loss / Q000502:physiology
chemical_list: D020738:Leptin; D012333:RNA, Messenger; D000685:Serum Amyloid A Protein