title: Serum adiponectin is decreased in patients with familial combined hyperlipidemia and normolipaemic relatives and is influenced by lipid-lowering treatment.
abstract: OBJECTIVE
  Hypoadiponectinemia has been reported in patients with familial combined hyperlipidemia (FCHL) presenting increased waist circumference and insulin resistance. However, no studies have evaluated this association in non-obese FCHL patients. Moreover, it is unclear whether correction of lipoprotein abnormalities may influence adiponectin levels in FCHL.
  
  
  RESULTS
  We have compared serum levels of adiponectin in 199 non-obese FCHL patients (BMI 25.96+/-3.7), 116 normolipaemic (NL) non-affected relatives (BMI 24.4+/-4.0) and 192 controls (BMI 28.0+/-7.4). In a subgroup of FCHL patients, changes in adiponectin levels after treatment with atorvastatin (n=22) or fenofibrate (n=26) were also evaluated. FCHL patients as well as their NL relatives showed lower serum adiponectin levels compared to controls (9.7+/-5.4 microg/mL, 10.7+/-5.3 microg/mL and 17.3+/-13.7microg/mL, respectively; p<0.0001 for all comparisons). After controlling for confounders, the strongest association with hypoadiponectinemia was observed with family history of FCHL, followed by HDL-C (negatively) and age (positively). These variables jointly explained 15% of the total variance of serum adiponectin levels. After 24-week of treatment, adiponectin was increased by 12.5% (p<0.05) by atorvastatin and was reduced by 10% by fenofibrate, resulting in a treatment difference of 22.5% in favor of atorvastatin (p<0.017).
  
  
  CONCLUSIONS
  FCHL patients showed lower serum adiponectin levels compared to controls. Also normolipaemic relatives of FCHL patients presented decreased levels of adiponectin, suggesting a possible common background in the determination of this abnormality. Overall, these observations indicate that hypoadiponectinemia may be an inherent characteristic of the FCHL phenotype. In FCHL patients hypoadiponectinemia may be partially corrected by atorvastatin but not by fenofibrate treatment.
authors.affiliation: Department of Clinical and Medical Therapy, Unit of Medical Therapy, University La Sapienza of Rome, Azienda Policlinico Umberto I, Viale del Policlinico 155, 00161 Rome, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Arca
authors.forename: V M
authors.initials: VM
authors.lastname: Cambuli
authors.forename: A
authors.initials: A
authors.lastname: Montali
authors.forename: F
authors.initials: F
authors.lastname: Sentinelli
authors.forename: E
authors.initials: E
authors.lastname: Filippi
authors.forename: F
authors.initials: F
authors.lastname: Campagna
authors.forename: F
authors.initials: F
authors.lastname: Quagliarini
authors.forename: R
authors.initials: R
authors.lastname: Antonini
authors.forename: S
authors.initials: S
authors.lastname: Romeo
authors.forename: M G
authors.initials: MG
authors.lastname: Baroni
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D017677:Age Distribution; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D005190:Family; D005260:Female; D011345:Fenofibrate / Q000627:therapeutic use*; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D006950:Hyperlipidemia, Familial Combined / Q000097:blood* / Q000188:drug therapy* / Q000235:genetics; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D015995:Prevalence; D011758:Pyrroles / Q000627:therapeutic use*; D016032:Randomized Controlled Trials as Topic; D055105:Waist Circumference; D055815:Young Adult
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D008076:Cholesterol, HDL; D006538:Heptanoic Acids; D000960:Hypolipidemic Agents; D011758:Pyrroles; D000069059:Atorvastatin; D011345:Fenofibrate