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. 1998 Nov;54(5):385-93.
doi: 10.1111/j.1399-0004.1998.tb03751.x.

Genetic variants of the human obesity (OB) gene in subjects with and without Prader-Willi syndrome: comparison with body mass index and weight

M G Butler  1 , L Hedges, C L Hovis, I D Feurer
Affiliations

Genetic variants of the human obesity (OB) gene in subjects with and without Prader-Willi syndrome: comparison with body mass index and weight

M G Butler et al. Clin Genet. 1998 Nov.

Abstract

We investigated whether an association exists between genetic variants of the human obesity (OB or leptin) gene and body mass index (BMI) or weight in subjects with Prader Willi syndrome (PWS) and in age- and gender-matched lean and obese subjects without PWS. The study included 51 subjects with PWS (mean age = 17.7 +/- 9.5 years, BMI = 29.7 +/- 8.3 kg/m2); 50 non-PWS obese subjects (mean age = 18.2 +/- 10.8 years, BMI = 33.3 +/- 9.5 kg/m2); and 53 non-PWS lean subjects (mean age = 17.8 +/- 9.5 years, BMI = 19.5 +/- 2.9 kg/m2). Allele sizes were determined via standard polymerase chain reaction of the D7S1875 locus, a dinucleotide repeat polymorphism close to the OB gene and classified as trichotomous (homozygous < 208 bp, heterozygous < 208/ > or = 208 bp, homozygous > or = 208 bp) or dichotomous (homozygous < 208 bp or not). Non-PWS males showed a marked decrease in weight with larger alleles while females did not (interaction effect, p < 0.05). Comparable effects were not observed among the PWS subjects. Associations between BMI and genotype were statistically significant (r = 0.22, one-tailed p < 0.05) and comparable to previous research among the non-PWS subjects < 18 years, but not the adults (r = 0.05, one-tailed p = 0.38). Correlations were not statistically significant among either the adult or non-adult PWS subjects.

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Figures

Fig. 1.
Fig. 1.
The distribution of D7S1875 allele sizes among PWS, lean, and obese subjects.
Fig. 2.
Fig. 2.
Average BMI across D7S1875 allele groups among PWS and control (lean and obese) subjects (top panel). Average weight across D7S1875 allele groups among PWS and control (lean and obese) subjects (bottom panel).
Fig. 3.
Fig. 3.
Average BMI across D7S1875 allele groups among PWS, lean, and obese control subjects (top panel). Average weight across D7S1875 allele groups among PWS, lean, and obese control subjects (bottom panel).
Fig. 4.
Fig. 4.
Average BMI across D7S1875 allele groups among PWS and control subjects by gender (top panel). Average weight across D7S1875 allele groups among PWS and control subjects by gender (bottom panel).
See this image and copyright information in PMC

References

    1. Cassidy SB. Prader–Willi syndrome. Curr Prob Pediatr 1984: 14: 1–55. - PubMed
    1. Butler MG, Meaney FJ, Palmer CG. Clinical and cytogenetic survey of 39 individuals with Prader-Labhart-Willi syndrome. Am J Med Genet 1986: 23: 793–809. - PMC - PubMed
    1. Butler MG. Prader–Willi syndrome: current understanding of cause and diagnosis. Am J Med Genet 1990: 35: 319–332. - PMC - PubMed
    1. Holm VA, Cassidy SB, Butler MG, Hanchett JM, Greenswag LR, Whitman BY, Greenberg F. Prader–Willi syndrome: consensus diagnostic criteria. Pediatrics 1993: 91: 398–402. - PMC - PubMed
    1. Butler MG, Levine GJ, Le JY, Hall BD, Cassidy SB. Photoanthropometric study of craniofacial traits of individuals with Prader–Willi syndrome. Am J Med Genet 1995: 58: 38–45. - PMC - PubMed

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