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WNT10B mutations in human obesity.

C Christodoulides1, A Scarda, M Granzotto

  • 1Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Box 232, Cambridge, CB2 2QQ, UK.

Diabetologia
|February 16, 2006
PubMed
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Mutations in the wingless-type MMTV integration site family, member 10B (WNT10B) gene were investigated for links to human obesity. A non-functioning WNT10B allele was identified in an obese family, suggesting a potential role in obesity development.

Area of Science:

  • Genetics
  • Molecular Biology
  • Obesity Research

Background:

  • Wingless-type MMTV integration site family, member 10B (WNT10B) is implicated in regulating adipocyte differentiation.
  • Understanding genetic factors contributing to human obesity is crucial for developing effective interventions.

Purpose of the Study:

  • To investigate whether mutations in the WNT10B gene contribute to human obesity.
  • To screen obese populations for novel WNT10B mutations.

Main Methods:

  • Screened two independent populations (UK and Italian) comprising 96 and 115 obese subjects, respectively, for WNT10B mutations.
  • Conducted functional analysis of identified WNT10B variants to assess their impact on WNT signaling and adipogenesis.
  • Performed pedigree analysis to evaluate cosegregation of variants with obesity within families.

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Main Results:

  • Identified one proband with early-onset obesity heterozygous for a C256Y WNT10B mutation that abrogated WNT signaling and blocked adipogenesis.
  • The C256Y mutation was absent in 600 control alleles, and all carriers in the proband's family were overweight or obese.
  • Three other rare missense variants were found, but only one (P301S) showed no functional impairment, and others did not clearly cosegregate with obesity.

Conclusions:

  • The identified C256Y mutation represents the first naturally occurring missense variant of WNT10B associated with impaired function.
  • While not definitive proof, the presence of a non-functioning WNT10B allele in an obese family warrants further investigation of WNT10B in other obese cohorts.
  • These findings highlight WNT10B as a potential candidate gene for obesity research.