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

Anne-Kathrin Wermter1, André Scherag, Katja Holter

  • 1Department of Child and Adolescent Psychiatry, University of Marburg, Germany.

Obesity Facts
|January 8, 2010
PubMed

Insights

Genetic variations in procolipase (CLPS) were not associated with early-onset obesity or dietary fat intake in children and adolescents. This study found no link between CLPS single nucleotide polymorphisms and obesity risk.

Area of Science:

  • Genetics
  • Human Physiology
  • Obesity Research

Background:

  • Procolipase (CLPS) and enterostatin are implicated in fat absorption and appetite regulation in rodents.
  • The role of CLPS genetic variations in human obesity and eating behavior remains largely unexplored.

Purpose of the Study:

  • To investigate the association between genetic variations in the CLPS gene and early-onset obesity.
  • To explore the relationship between CLPS genetic variations and dietary fat intake in humans.

Main Methods:

  • Screening of CLPS for sequence variations in extremely obese children/adolescents and underweight young adults.
  • Genotyping of single nucleotide polymorphisms (SNPs) in obese and control groups.
  • Case-control and family-based association analyses were conducted.

Main Results:

  • Five CLPS sequence variations were identified, including two non-synonymous SNPs (rs2766597, rs41270082) and one 5'UTR SNP (rs3748050).
  • No significant association was found between CLPS SNPs (rs2766597, rs3748050, rs3748051) and obesity.
  • A trend for association with rs41270082 was not substantiated; no association was observed with dietary fat intake percentages.

Conclusions:

  • The studied CLPS single nucleotide polymorphisms (SNPs) showed no evidence of association with obesity in children and adolescents.
  • No significant link was established between CLPS genetic variations and the percentage of dietary fat intake.
  • Further research may be needed to fully elucidate the role of CLPS in human metabolism and weight regulation.
Abstract

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