Procolipase gene: no association with early-onset obesity or fat intake

Anne-Kathrin Wermter, André Scherag, Katja Holter, Kathrin Reichwald, Peter Lichtner, Wolfgang Siegfried, John Blundell, Clare Lawton, Stephen Whybrow, James Stubbs, Jonathan R Arch, Thomas Meitinger, Matthias Platzer, Anke Hinney, Johannes Hebebrand

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Abstract

Background: Several lines of evidence in volvement of procolipase (CLPS) or its derivative enterostatin in dietary fat absorption, regulation of fat intake, and body weight in rodents. We explored the relationship between genetic variation in CLPS, early-onset obesity and fat intake in humans. Methods: We screened the CLPS in 93 extremely obese children and adolescents and 96 underweight young adults for sequence variations and genotyped single nucleotide polymorphisms (SNPs) in extremely obese children and adolescents, healthy normal-and underweight young adults and obesity trios. Case-control and family-based association analyses were performed. Results: Five sequence variations were identified: two non-synonymous SNPs: rs2766597 (Leu8Pro), rs41270082 (Arg109Cys); one SNP in the 5′UTR: rs3748050; one intronic SNP: rs3748051; and one infrequent novel non-synonymous variant: Arg55His. For rs2766597, rs3748050, and rs3748051 we obtained no evidence for an association with obesity in the case-control comparison. For rs41270082 there was a trend for association which could not be substantiated in the family-based association analysis. Additionally, we found no association in subgroup analyses pertaining to the extremely obese children and adolescents in the lowest and highest quartile of the percentage of energy consumed as fat. Conclusions: We found no evidence for an association of CLPS SNPs rs2766597, rs41270082, rs3748050, and rs3748051 with obesity or percentage of dietary fat intake.
Original languageEnglish
Pages (from-to)40-44
Number of pages5
JournalObesity Facts
Volume2
Issue number1
DOIs
Publication statusPublished - Feb 2009

Fingerprint

Single Nucleotide Polymorphism
Obesity
Fats
adolescent
young adult
Thinness
Genes
Dietary Fats
evidence
body weight
Young Adult
energy
regulation
trend
Rodentia
Body Weight
procolipase

Keywords

  • adolescent
  • adult
  • case-control studies
  • child
  • colipases
  • dietary fats
  • enzyme precursors
  • family
  • female
  • genotype
  • humans
  • male
  • middle aged
  • mutation
  • obesity
  • polymorphism, single nucleotide

Cite this

Wermter, A-K., Scherag, A., Holter, K., Reichwald, K., Lichtner, P., Siegfried, W., ... Hebebrand, J. (2009). Procolipase gene: no association with early-onset obesity or fat intake. Obesity Facts, 2(1), 40-44. https://doi.org/10.1159/000196379

Procolipase gene : no association with early-onset obesity or fat intake. / Wermter, Anne-Kathrin; Scherag, André; Holter, Katja; Reichwald, Kathrin; Lichtner, Peter; Siegfried, Wolfgang; Blundell, John; Lawton, Clare; Whybrow, Stephen; Stubbs, James; Arch, Jonathan R; Meitinger, Thomas; Platzer, Matthias; Hinney, Anke; Hebebrand, Johannes.

In: Obesity Facts, Vol. 2, No. 1, 02.2009, p. 40-44.

Research output: Contribution to journalArticle

Wermter, A-K, Scherag, A, Holter, K, Reichwald, K, Lichtner, P, Siegfried, W, Blundell, J, Lawton, C, Whybrow, S, Stubbs, J, Arch, JR, Meitinger, T, Platzer, M, Hinney, A & Hebebrand, J 2009, 'Procolipase gene: no association with early-onset obesity or fat intake', Obesity Facts, vol. 2, no. 1, pp. 40-44. https://doi.org/10.1159/000196379
Wermter A-K, Scherag A, Holter K, Reichwald K, Lichtner P, Siegfried W et al. Procolipase gene: no association with early-onset obesity or fat intake. Obesity Facts. 2009 Feb;2(1):40-44. https://doi.org/10.1159/000196379
Wermter, Anne-Kathrin ; Scherag, André ; Holter, Katja ; Reichwald, Kathrin ; Lichtner, Peter ; Siegfried, Wolfgang ; Blundell, John ; Lawton, Clare ; Whybrow, Stephen ; Stubbs, James ; Arch, Jonathan R ; Meitinger, Thomas ; Platzer, Matthias ; Hinney, Anke ; Hebebrand, Johannes. / Procolipase gene : no association with early-onset obesity or fat intake. In: Obesity Facts. 2009 ; Vol. 2, No. 1. pp. 40-44.
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abstract = "Background: Several lines of evidence in volvement of procolipase (CLPS) or its derivative enterostatin in dietary fat absorption, regulation of fat intake, and body weight in rodents. We explored the relationship between genetic variation in CLPS, early-onset obesity and fat intake in humans. Methods: We screened the CLPS in 93 extremely obese children and adolescents and 96 underweight young adults for sequence variations and genotyped single nucleotide polymorphisms (SNPs) in extremely obese children and adolescents, healthy normal-and underweight young adults and obesity trios. Case-control and family-based association analyses were performed. Results: Five sequence variations were identified: two non-synonymous SNPs: rs2766597 (Leu8Pro), rs41270082 (Arg109Cys); one SNP in the 5′UTR: rs3748050; one intronic SNP: rs3748051; and one infrequent novel non-synonymous variant: Arg55His. For rs2766597, rs3748050, and rs3748051 we obtained no evidence for an association with obesity in the case-control comparison. For rs41270082 there was a trend for association which could not be substantiated in the family-based association analysis. Additionally, we found no association in subgroup analyses pertaining to the extremely obese children and adolescents in the lowest and highest quartile of the percentage of energy consumed as fat. Conclusions: We found no evidence for an association of CLPS SNPs rs2766597, rs41270082, rs3748050, and rs3748051 with obesity or percentage of dietary fat intake.",
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AU - Wermter, Anne-Kathrin

AU - Scherag, André

AU - Holter, Katja

AU - Reichwald, Kathrin

AU - Lichtner, Peter

AU - Siegfried, Wolfgang

AU - Blundell, John

AU - Lawton, Clare

AU - Whybrow, Stephen

AU - Stubbs, James

AU - Arch, Jonathan R

AU - Meitinger, Thomas

AU - Platzer, Matthias

AU - Hinney, Anke

AU - Hebebrand, Johannes

N1 - Copyright 2009 S. Karger AG, Basel.

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N2 - Background: Several lines of evidence in volvement of procolipase (CLPS) or its derivative enterostatin in dietary fat absorption, regulation of fat intake, and body weight in rodents. We explored the relationship between genetic variation in CLPS, early-onset obesity and fat intake in humans. Methods: We screened the CLPS in 93 extremely obese children and adolescents and 96 underweight young adults for sequence variations and genotyped single nucleotide polymorphisms (SNPs) in extremely obese children and adolescents, healthy normal-and underweight young adults and obesity trios. Case-control and family-based association analyses were performed. Results: Five sequence variations were identified: two non-synonymous SNPs: rs2766597 (Leu8Pro), rs41270082 (Arg109Cys); one SNP in the 5′UTR: rs3748050; one intronic SNP: rs3748051; and one infrequent novel non-synonymous variant: Arg55His. For rs2766597, rs3748050, and rs3748051 we obtained no evidence for an association with obesity in the case-control comparison. For rs41270082 there was a trend for association which could not be substantiated in the family-based association analysis. Additionally, we found no association in subgroup analyses pertaining to the extremely obese children and adolescents in the lowest and highest quartile of the percentage of energy consumed as fat. Conclusions: We found no evidence for an association of CLPS SNPs rs2766597, rs41270082, rs3748050, and rs3748051 with obesity or percentage of dietary fat intake.

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KW - enzyme precursors

KW - family

KW - female

KW - genotype

KW - humans

KW - male

KW - middle aged

KW - mutation

KW - obesity

KW - polymorphism, single nucleotide

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JO - Obesity Facts

JF - Obesity Facts

SN - 1662-4025

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