ArticleEndocrine2013
Mutation analysis of WNT10B in obese children, adolescents and adults.
Article in Endocrine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Nucleotide variation of sFRP5 gene is not associated with obesity in children and adolescents.Molecular biology reports · 2016Article
- Wnt signaling and the control of human stem cell fate.Stem cell reviews and reports · 2014Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wingless-type MMTV integration site family, member 10B (WNT10B) is an activator of the Wnt pathway. The Wnt pathway is known to play an important role in maintenance and differentiation of stem cells and has been implicated in the origination of obesity. To evaluate the role of genetic variation in WNT10B in obesity further, we performed a mutation analysis on Belgian obese patients and control subjects. A mutation analysis of WNT10B by means of high-resolution melting curve analysis and direct sequencing was performed on 546 obese children and adolescents (mean Z-score of 2.6 ± 0.6 and 2.5 ± 0.4 respectively), 86 morbidly obese adults (mean BMI of 48.0 ± 0.4 kg/m(2)) and 447 lean, healthy controls (mean BMI of 22.1 ± 1.7 kg/m(2)). A total of five novel non-synonymous variants were identified. R228Q was the only coding, non-synonymous variant that was exclusively found in patients, but the variant did not co-segregate with obesity in the three investigated siblings. The remaining four variants were either found both in cases and in control samples (G181D) or only in control samples (A108P, S187R and P315S). The frequency of non-synonymous variants in lean individuals (0.9 %) was higher than in obese individuals (0.3 %) and familial co-segregation of the most promising variant in patients could not be demonstrated. Therefore, we conclude that variations in WNT10B do not contribute to human monogenic obesity in our population.
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