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  • 1
    Electronic Resource
    Electronic Resource
    Homozygosity of the Pro12Ala variant of the peroxisome proliferation-activated receptor-γ2 (PPAR-γ2): divergent modulating effects on body mass index in obese and lean Caucasian men (1999)
    Springer
    Diabetologia 42 (1999), S. 892-895 
    Details
    ISSN: 1432-0428
    Keywords: Keywords PPAR-γ2 ; mutations ; obesity ; body mass index changes ; epidemiology.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. The objectives of the present investigation were to examine: 1) whether a Pro115Gln variant in the peroxisome proliferator-activated receptor-γ2 (PPAR- γ 2) is associated with juvenile-onset obesity among Danish Caucasianmen and 2) whether the relation of a Pro12Ala polymorphism in PPAR- γ 2 with BMI and long-term weight regulation differ between lean and obese subjects within the same cohort. Methods. The Pro115Gln and Pro112Ala variants were examined using PCR and RFLP in a group of 752 subjects with a Body Mass Index (BMI) of 31.0 kg/m2 or more and in 869 non-obese control subjects. Results. We did not find Pro115Gln in any of the 1621 male subjects we examined. Among the males with juvenile-onset obesity, the allelic frequency of the Pro12Ala polymorphism was 14 % (95 % confidence interval: 12–16 %) compared with 16 % (14–17 %) among the non-obese control subjects (NS). Heterozygosity of the codon 12 variant was not associated with differences in BMI or changes in body weight regulation during follow up in lean or obese subjects. In the group of obese subjects, 21 homozygous Ala12Ala carriers had, however, a higher BMI (38.9 ± 5.4 kg/m2 (means ± SD) vs 35.5 ± 5.5 kg/m2, p = 0.008) and a higher weight gain (0.27 ± 0.24 kg · m–2· year–1 vs 0.10 ± 0.24 kg · m–2· year–1, p = 0.004), compared with wild-type carriers. Moreover, within the control group of 869 men the 14 homozygous carriers of the variant had a lower BMI (24.4 ± 2.7 kg/m2 vs 26.2 ± 3.7 kg/m2, p = 0.005) and a slower increase in BMI (0.11 ± 0.11 kg · m–2· year–1 vs 0.17 ± 0.11 kg · m–2· year–1, p = 0.002) compared with wild-type carriers. Conclusion/interpretation. The codon 12 variant of PPAR- γ 2 is not intrinsically associated with juvenile obesity. The variant may in its homozygous form interact, however, with various combinations of genetic and environmental factors in lean and obese subjects to cause divergent modulating effects on BMI and long-term body weight control. [Diabetologia (1999) 42: 892–895]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051243
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  • 2
    Electronic Resource
    Electronic Resource
    Mutational analysis of the coding region of the uncoupling protein 2 gene in obese NIDDM patients: Impact of a common amino acid polymorphism on juvenile and maturity onset forms of obesity and insulin resistance (1997)
    Springer
    Diabetologia 40 (1997), S. 1227-1230 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Uncoupling protein 2 ; obesity ; genetics ; insulin resistance ; amino acid polymorphism.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recently, a gene encoding a novel human uncoupling protein, designated UCP2, was discovered. The murine UCP2 was mapped to a region on mouse chromosome 7 which in several models has been shown to be linked to obesity and hyperinsulinaemia. Single strand conformation polymorphism (SSCP) analysis and direct sequencing of the coding region of the UCP2 gene in 35 obese Caucasian NIDDM patients of Danish ancestry revealed one nucleotide substitution, replacing an alanine with a valine at codon 55. The amino acid polymorphism was present in 24 of the 35 (69 %) examined subjects. The allelic frequency of the A/V55 variant was 48.3 % (95 % CI: 42.5–54.1 %) among 144 subjects with juvenile onset obesity, 45.6 % (40.5–50.7 %) among 182 subjects randomly selected at the draft board examination, and 45.5 % (37.1–53.9 %) among lean control subjects selected from the same study cohort. Within these cohorts there were no differences in BMI values at different ages among wild-type carriers and A/V55 carriers. In a population-based sample of 369 young healthy Caucasians the variant showed no association with alterations in BMI, waist-to-hip ratio, fat mass or weight gain during childhood or adolescence. The A/V55 polymorphism was not related to alterations in fasting values of serum insulin and C-peptide or to an impaired insulin sensitivity index. We conclude that genetic variability in the human UCP2 gene is not a common factor contributing to NIDDM in obese Danish Caucasian subjects and the common A/V55 amino acid polymorphism of the gene is not implicated in the pathogenesis of juvenile or maturity onset obesity or insulin resistance in Caucasians. [Diabetologia (1997) 40: 1227–1230]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050811
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Organisation of the coding exons and mutational screening of the uncoupling protein 3 gene in subjects with juvenile-onset obesity (1998)
    Springer
    Diabetologia 41 (1998), S. 241-244 
    Details
    ISSN: 1432-0428
    Keywords: Keywords uncoupling protein 3 ; obesity ; genetics ; mutation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Uncoupling proteins (UCPs) are mitochondrial transporters that uncouple the cellular respiration releasing stored energy as heat. Recently a third member of the UCP family was identified. Human UCP3 is different from UCP1 and UCP2 by its high and preferential expression in skeletal muscle and consequently the UCP3 gene is an attractive candidate gene for obesity. In this study we have determined the intron/exon organization of the coding region of the UCP3 gene and performed single strand conformation polymorphism (SSCP) analysis and direct sequencing of variants of the gene in 60 Caucasian subjects with juvenile-onset obesity. We detected 4 nucleotide substitutions in the intron regions and 2 silent amino acid variants. During the identification of the intron/exon structure of the gene in a normal healthy male subject with a BMI of 23.5 kg/m2, a nucleotide substitution replacing a glycine with a serine was identified at codon 84. This variant was neither found among 156 subjects with juvenile-onset obesity nor among 205 control subjects. In a population based sample of 380 young healthy subjects the Gly/Ser84 variant was found in one female subject with a BMI of 25.5 kg/m2 and a fat mass of 23.7 kg. We conclude it is unlikely that variants in the coding region of the UCP3 gene contribute to the pathogenesis of juvenile-onset obesity among Danish Caucasians. [Diabetologia (1998) 41: 241–244]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050897
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    Paper (German National Licenses)
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