title: Relationship between perilipin gene polymorphisms and body weight and body   composition during weight loss and weight maintenance.
abstract: BACKGROUND
  Genetic variation in the perilipin (PLIN) gene may play a role in the etiology and treatment of obesity.
  
  
  OBJECTIVE
  To examine different polymorphisms in the PLIN gene in relation to body-weight regulation.
  
  
  METHODS
  118 subjects followed a 6 wk VLCD, followed by 1 year weight maintenance. Body-weight (BW), body composition, leptin concentration, and polymorphisms of the PLIN gene: PLIN1:rs2289487, PLIN4:rs894160, PLIN6:rs1052700, PLIN5:rs2304795 and PLIN7:rs 2304796 were determined.
  
  
  RESULTS
  BW loss during VLCD was 7.0+/-3.1 kg (p<0.05), and BW regain was 3.7+/-1.4 kg (p<0.05), including changes in body mass index (BMI), waist-circumference, body-composition and leptin concentrations (p<0.05). Linkage disequilibria were observed between PLIN1 and PLIN4: D' >0.9, r2=0.72; PLIN5 and PLIN7: D' >0.9, r2=0.85. In men, body weight, BMI, waist circumference, body fat, leptin concentrations were significantly lower for the haplotype of PLIN1 (C-alleles) and PLIN4 (A-alleles). In women weight loss and loss of fat mass were larger for the haplotype of PLIN1 (C-alleles) and PLIN4 (A-alleles). For PLIN6 genotypes body weight and body fat were lower for homozygotes of the minor allele (T/T) in the men; in the women leptin concentrations were lower. The haplotype of PLIN5 and PLIN7 consisting of A/G and G/G of PLIN5 and A/A of PLIN7 showed a reduction in FM: 5.9+/-0.6 kg vs 3.1+/-0.4 kg, % body fat: 5.5+/-0.6% vs 2.2+/-0.2%, and leptin: 20.5+/-10.8 ng/ml vs 12.9+/-6.7 ng/ml over time in the women (p<0.05).
  
  
  CONCLUSIONS
  Since the haplotype of the minor alleles PLIN1-4, PLIN5-7 and PLIN6, was related to body-weight regulation at a lower level of body-weight in the men as well in the women we conclude that the PLIN1-4, 6, and 5-7 locus appears as a genetic influencer of obesity risk in humans.
authors.affiliation: Department of Human Biology, Maastricht University, P.O. Box 616, Maastricht 6200 MD, The Netherlands.
authors.forename: Stijn
authors.initials: S
authors.lastname: Soenen
authors.forename: Edwin C M
authors.initials: EC
authors.lastname: Mariman
authors.forename: Neeltje
authors.initials: N
authors.lastname: Vogels
authors.forename: Freek G
authors.initials: FG
authors.lastname: Bouwman
authors.forename: Marcel
authors.initials: M
authors.lastname: den Hoed
authors.forename: Louise
authors.initials: L
authors.lastname: Brown
authors.forename: Margriet S
authors.initials: MS
authors.lastname: Westerterp-Plantenga
mesh_terms: D000328:Adult; D001823:Body Composition / Q000235:genetics* / Q000502:physiology; D001835:Body Weight / Q000235:genetics; D002352:Carrier Proteins; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000235:genetics*; D000070778:Perilipin-1; D010750:Phosphoproteins / Q000235:genetics*; D012307:Risk Factors; D015431:Weight Loss / Q000235:genetics* / Q000502:physiology
chemical_list: D002352:Carrier Proteins; D020738:Leptin; C000602978:PLIN1 protein, human; D000070778:Perilipin-1; D010750:Phosphoproteins