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  • 1
    Online-Ressource
    Online-Ressource
    Factors of Insulin Resistance Syndrome–Related Phenotypes Are Linked to Genetic Locations on Chromosomes 6 and 7 in Nondiabetic Mexican-Americans
    American Diabetes Association ; 2002
    In:  Diabetes Vol. 51, No. 3 ( 2002-03-01), p. 841-847
    Details
    In: Diabetes, American Diabetes Association, Vol. 51, No. 3 ( 2002-03-01), p. 841-847
    Kurzfassung: Insulin resistance syndrome (IRS)−related phenotypes, such as hyperinsulinemia, obesity-related traits, impaired glucose tolerance, dyslipidemia, and hypertension, tend to cluster into factors. We attempted to identify loci influencing the factors of IRS-related phenotypes using phenotypic data from 261 nondiabetic subjects distributed across 27 low-income Mexican-American extended families. Principal component factor analyses were performed using eight IRS-related phenotypes: fasting glucose (FG), fasting specific insulin (FSI), BMI, systolic blood pressure (SBP), diastolic blood pressure (DBP), HDL cholesterol, ln triglycerides (ln TGs), and leptin (LEP). The factor analysis yielded three factors: factor 1 (BMI, LEP, and FSI), factor 2 (DBP and SBP), and factor 3 (HDL and ln TG). We conducted multipoint variance components linkage analyses on these factors with the program SOLAR using a 10–15 cM map. We found significant evidence for linkage of factor 1 to two regions on chromosome 6 near markers D6S403 (logarithm of odds [LOD] = 4.2) and D6S264 (LOD = 4.9). We also found strong evidence for linkage of factor 3 to a genetic location on chromosome 7 between markers D7S479 and D7S471 (LOD = 3.2). In conclusion, we found substantial evidence for susceptibility loci on chromosomes 6 and 7 that appear to influence the factors representing the IRS-related phenotypes in Mexican-Americans.
    Materialart: Online-Ressource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.51.3.841
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2002
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 2
    Online-Ressource
    Online-Ressource
    Evidence for a Major Gene for Type II Diabetes and Linkage Analyses With Selected Candidate Genes in Mexican-Americans
    American Diabetes Association ; 1996
    In:  Diabetes Vol. 45, No. 5 ( 1996-05-01), p. 563-568
    Details
    In: Diabetes, American Diabetes Association, Vol. 45, No. 5 ( 1996-05-01), p. 563-568
    Kurzfassung: We have carried out two independent family studies in low-income Mexican-Americans from San Antonio, Texas. In the first study, probands were ascertained at random without regard to any medical condition (658 examined individuals from 50 families), and in the second study, probands were subjects with type II diabetes identified in a prior epidemiological survey (523 examined individuals from 29 families). Pedigrees ranging in size from 2 to 45 family members (median 11) in the first study and from 2 to 50 family members (median 12) in the second study were examined. Diabetes was diagnosed according to World Health Organization criteria. In both sets of families, segregation analyses revealed support for a major gene with an autosomal dominant mode of inheritance influencing early age of onset of diabetes. Non-Mendelian inheritance was rejected in both data sets. Individuals with the early age of onset allele had a mean age of diabetes onset of 51 years in the first data set and 60 years in the second data set. In the first data set, the major gene accounted for ∼70% of the phenotypic variance in age of onset of diabetes, and there were no residual family effects once the major gene effect was taken into account. In the second data set, the major gene accounted for ∼50% of the phenotypic variance, and residual family effects were statistically significant. Linkage analyses were performed with 11 candidate genes, and tight linkage with diabetes was rejected for Rh blood group, glucose transporter 2, fatty acid–binding protein, tumor necrosis factor β, glucokinase, and lipoprotein lipase. A logarithm of odds (LOD) score of 0.92 at a recombination fraction of 0.05 was observed for insulin receptor substrate 1. This LOD score corresponds to a χ2 of 4.24 (P = 0.039).
    Materialart: Online-Ressource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diab.45.5.563
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 1996
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 3
    Online-Ressource
    Online-Ressource
    Evidence for Linkage of Postchallenge Insulin Levels With Intestinal Fatty Acid-Binding Protein (FABP2) in Mexican-Americans
    American Diabetes Association ; 1995
    In:  Diabetes Vol. 44, No. 9 ( 1995-09-01), p. 1046-1053
    Details
    In: Diabetes, American Diabetes Association, Vol. 44, No. 9 ( 1995-09-01), p. 1046-1053
    Kurzfassung: Single genes with large effects may contribute to insulin resistance or influence susceptibility to non-insulin-dependent diabetes mellitus (NIDDM). In the Pima Indians, results from sib-pair analysis have suggested that a gene on chromosome 4q influences both fasting insulin levels and maximal insulin action. We conducted sib-pair and logarithm of odds (LOD)-score linkage analysis to seek evidence for linkage between genes influencing insulin levels and chromosome 4q loci. Analyses were conducted on nondiabetic individuals from 28 different families participating in the San Antonio Family Diabetes Study. All subjects received a 2-h oral glucose tolerance test. Fasting insulin levels were measured in 382 nondiabetic individuals, and 2-h insulin levels were measured in 366 individuals. Initial sib-pair linkage analysis revealed a possible association between 2-h post–glucose challenge insulin levels and the intestinal fatty acid–binding protein (FABP2) locus located in the region of chromosome 4q28–31 (P = 0.006). Subsequent sib-pair linkage analysis of 11 additional chromosome 4q markers supported this hypothesis. We next conducted segregation analyses to estimate allele frequencies and other model parameters for the putative locus influencing 2-h insulin levels. Results of LOD-score linkage analysis indicated possible linkage between the major gene described by the segregation model and FABP2. Using combined segregation and linkage analysis, we obtained a LOD-score of 2.80 at recombination frequency of 0.0 between FABP2 and the putative locus influencing 2-h insulin levels. The maximum likelihood estimate of the allele associated with low insulin levels was 0.21. Individuals having one or two copies of this allele had a mean ln(2-h insulin level) equal to 3.484 (back-transformed mean = 298.4 pmol/1), compared with 4.480 (back-transformed mean = 807.8 pmol/1) for individuals in whom this allele was absent. Approximately 32% of the total phenotypic variance in ln(2-h insulin levels) could be attributed to this locus. These results are consistent with the hypothesis that FABP2, or a tightly linked gene, influences 2-h insulin levels. This gene may be associated with insulin resistance.
    Materialart: Online-Ressource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diab.44.9.1046
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 1995
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 4
    Online-Ressource
    Online-Ressource
    Genome-Wide Association Study of the Modified Stumvoll Insulin Sensitivity Index Identifies BCL2 and FAM19A2 as Novel Insulin Sensitivity Loci
    American Diabetes Association ; 2016
    In:  Diabetes Vol. 65, No. 10 ( 2016-10-01), p. 3200-3211
    Details
    In: Diabetes, American Diabetes Association, Vol. 65, No. 10 ( 2016-10-01), p. 3200-3211
    Kurzfassung: Genome-wide association studies (GWAS) have found few common variants that influence fasting measures of insulin sensitivity. We hypothesized that a GWAS of an integrated assessment of fasting and dynamic measures of insulin sensitivity would detect novel common variants. We performed a GWAS of the modified Stumvoll Insulin Sensitivity Index (ISI) within the Meta-Analyses of Glucose and Insulin-Related Traits Consortium. Discovery for genetic association was performed in 16,753 individuals, and replication was attempted for the 23 most significant novel loci in 13,354 independent individuals. Association with ISI was tested in models adjusted for age, sex, and BMI and in a model analyzing the combined influence of the genotype effect adjusted for BMI and the interaction effect between the genotype and BMI on ISI (model 3). In model 3, three variants reached genome-wide significance: rs13422522 (NYAP2; P = 8.87 × 10−11), rs12454712 (BCL2; P = 2.7 × 10−8), and rs10506418 (FAM19A2; P = 1.9 × 10−8). The association at NYAP2 was eliminated by conditioning on the known IRS1 insulin sensitivity locus; the BCL2 and FAM19A2 associations were independent of known cardiometabolic loci. In conclusion, we identified two novel loci and replicated known variants associated with insulin sensitivity. Further studies are needed to clarify the causal variant and function at the BCL2 and FAM19A2 loci.
    Materialart: Online-Ressource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db16-0199
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2016
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
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