title: Decrease of Lp(a) during weight reduction in obese children is modified by the apo(a) kringle-IV copy number variation.
abstract: BACKGROUND
  Lipoprotein(a) [Lp(a)] is considered an independent risk factor for cardiovascular disease. Its concentration is mainly determined by the kringle-IV repeat copy number variation (CNV) at the apolipoprotein(a) [apo(a)] locus.
  
  
  OBJECTIVE
  We aimed to investigate the immediate effect of weight reduction on plasma Lp(a) levels and its dependency on the apo(a) CNV in obese children.
  
  
  METHODS
  We performed a prospective longitudinal intervention study of a low-fat hypocaloric diet conducted in a 3-week dietary camp for obese children. In all, 140 obese participants (54 boys and 86 girls) with a mean age of 12.5+/-1.6 years and a mean relative body mass index (BMI) before treatment of 165.6+/-24.7% were included. Body weight and plasma levels of Lp(a), lipids, apolipoproteins A-I and B, insulin, and C-reactive protein were determined before the onset and after the end of the intervention. In addition, the number of apo(a) kringle-IV repeats were determined using sodium dodecyl sulfate agarose gel electrophoresis.
  
  
  RESULTS
  The mean loss of body weight was 5.0+/-1.3 kg (-6.6%), resulting in a mean decrease of the relative BMI of 6.6%. Blood chemistry revealed significant changes in all parameters, especially in Lp(a), with a decrease from 24.4+/-30.6 to 17.9+/-22.6 mg per 100 ml or -19% (P<0.001). The decrease of Lp(a) levels was higher in the group with low compared with high molecular weight apo(a) phenotypes (-23.9 vs -16.6%).
  
  
  CONCLUSIONS
  Weight reduction in obese children is associated with significant changes in Lp(a) levels, especially in subjects with high pre-treatment Lp(a) concentrations. This effect is markedly influenced by the molecular phenotype at the copy-number variable apo(a) locus.
authors.affiliation: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Schöpfstrasse, Innsbruck, Austria.
authors.forename: A
authors.initials: A
authors.lastname: Brandstätter
authors.forename: A
authors.initials: A
authors.lastname: Lingenhel
authors.forename: K
authors.initials: K
authors.lastname: Zwiauer
authors.forename: W
authors.initials: W
authors.lastname: Strobl
authors.forename: F
authors.initials: F
authors.lastname: Kronenberg
mesh_terms: D000293:Adolescent; D001054:Apolipoproteins A / Q000097:blood* / Q000235:genetics; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000097:blood* / Q000235:genetics; D002648:Child; D018752:Diet, Fat-Restricted; D005260:Female; D006801:Humans; D018082:Kringles / Q000235:genetics / Q000502:physiology*; D017270:Lipoprotein(a) / Q000097:blood* / Q000235:genetics; D008137:Longitudinal Studies; D008297:Male; D009765:Obesity / Q000097:blood* / Q000235:genetics; D010641:Phenotype; D011446:Prospective Studies; D012307:Risk Factors; D015431:Weight Loss / Q000235:genetics / Q000502:physiology*
chemical_list: D001054:Apolipoproteins A; D017270:Lipoprotein(a)