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  • 1
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    The Gly(972)Arg Variant of Human IRS1 Gene Is Associated With Variation in Glomerular Filtration Rate Likely Through Impaired Insulin Receptor Signaling
    American Diabetes Association ; 2012
    In:  Diabetes Vol. 61, No. 9 ( 2012-09-01), p. 2385-2393
    Details
    In: Diabetes, American Diabetes Association, Vol. 61, No. 9 ( 2012-09-01), p. 2385-2393
    Abstract: The objective of this study is to identify and characterize the genetic variants related to the glomerular filtration rate (GFR) linkage on 2q37. Of the positional candidate genes, we selected IRS1 and resequenced its 2-kb promoter region and exons for sequence variants in 32 subjects. A total of 11 single nucleotide polymorphisms (SNPs) were identified. To comprehensively cover the 59-kb-long intron-1, eight additional tagging SNPs were selected from the HapMap. All the 19 SNPs were genotyped by TaqMan Assay in the entire data set (N = 670; 39 families). Association analyses between the SNPs and GFR and type 2 diabetes–related traits were performed using the measured genotype approach. Of the SNPs examined for association, only the Gly(972)Arg variant of IRS1 exhibited a significant association with GFR (P = 0.0006) and serum triglycerides levels (P = 0.003), after accounting for trait-specific covariate effects. Carriers of Arg972 had significantly decreased GFR values. Gly(972)Arg contributed to 26% of the linkage signal on 2q. Expression of IRS1 mutant Arg972 in human mesangial cells significantly reduced the insulin-stimulated phosphorylation of IRS1 and Akt kinase. Taken together, the data provide the first evidence that genetic variation in IRS1 may influence variation in GFR probably through impaired insulin receptor signaling.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db11-1078
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2012
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  • 2
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    1717-P: Burden of Type 2 Diabetes and Its Genetic Determinants in Indian Populations: Findings from the INDIGENIUS Consortium
    American Diabetes Association ; 2019
    In:  Diabetes Vol. 68, No. Supplement_1 ( 2019-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: To address the public health issue of type 2 diabetes (T2D) and its genetic profile in India, we aimed to evaluate genetic determinants of T2D using family-based cohorts from four distinct Endogamous Ethnic Groups (EEGs) representing two Northern (Punjab [Sikhs: SI] and Rajasthan [Agarwals: AG] ) and two Southern (Tamil Nadu [Chettiars: CH] and Andhra Pradesh [Reddys: RE] ) states of India, and to examine whether genetic variants found through targeted sequencing of the previously established 8 South Asian T2D risk loci (including the one from the Sikh population) are relevant to the AG, CH, and RE EEGs. In this study, we report the findings of T2D occurrence and genetic basis of T2D/related traits from the EEGs, as part of the INDIGENIUS (Indian Diabetes Genetic Studies in collaboration with U.S.) consortium studies, supported by an Indo-U.S. Collaborative Research Partnership on T2D. Data and samples were collected from three EEGs: AG (N=530, Families=25, mean age=43y, mean BMI=27, T2D=37%); CH (N=518, families=21, Age=47y, BMI=27, T2D=33%), and RE (N=500, Families=22, Age=46y, BMI=27, T2D=36%). Each of the families from an EEG was ascertained by a proband with T2D. The status of T2D was defined by ADA 2018 guidelines (fasting glucose≥126 mg/dl or HbA1c≥6.5% and/or use of diabetes medication/history). Similar characteristics for the SI EEG (N=1260, Families=324, Age=51y, BMI=27, T2D=75%) were obtained previously. We used the variance components method as implemented in the program SOLAR to carry out genetic analyses. All analyses were adjusted for age and sex effects. In all cohorts, T2D heritability (h2) (p & lt;0.05) ranged from 30% (CH) to 81% (AG). Other T2D-related traits (e.g., BMI, lipids, blood pressure, insulin, glucose) in AG, CH, and RE EEGs exhibited strong genetic influences (h2 range: 15% [triglycerides] - 90% [glucose; non-T2D] ). Our findings highlight high burden of T2D in Indian EEGs with significant additive genetic influences on T2D and its related traits. Disclosure V. Venkatesan: None. J.C. Lopez-Alvarenga: None. R. Arya: None. T. Koshy: None. U. Ravichandran: None. S. Sharma: None. S. Lodha: None. A.R. Ponnala: None. K.K. Sharma: None. M.V. Shaik: None. R.G. Resendez: None. D. Ramu: None. P. Venugopal: None. P. R.: None. N. S.: None. J.A. Ezeilo: None. C.A. Bejar: None. S. Mummidi: None. C. Natesan: None. J. Blangero: None. K.M. Medicherla: None. S. Thanikachalam: None. T. Sadras Panchatcharam: None. D. K.: None. R. Gupta: None. D.K. Sanghera: None. R. Duggirala: None. S.F. Paul: None. Funding Indian Council of Medical Research (55/6/2/Indo-US/2014-NCD-II); National Institute of Diabetes and Digestive and Kidney Diseases (R21DK105913)
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-1717-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
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  • 3
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    Haplotypes of Transcription Factor 7–Like 2 ( TCF7L2 ) Gene and Its Upstream Region Are Associated With Type 2 Diabetes and Age of Onset in Mexican Americans
    American Diabetes Association ; 2007
    In:  Diabetes Vol. 56, No. 2 ( 2007-02-01), p. 389-393
    Details
    In: Diabetes, American Diabetes Association, Vol. 56, No. 2 ( 2007-02-01), p. 389-393
    Abstract: TCF7L2 acts as both a repressor and transactivator of genes, as directed by the Wnt signaling pathway. Recently, several highly correlated sequence variants located within a haplotype block of the TCF7L2 gene were observed to associate with type 2 diabetes in three Caucasian cohorts. We previously reported linkage of type 2 diabetes in the San Antonio Family Diabetes Study (SAFADS) cohort consisting of extended pedigrees of Mexican Americans to the region of chromosome 10q harboring TCF7L2. We therefore genotyped 11 single nucleotide polymorphisms (SNPs) from nine haplotype blocks across the gene in 545 SAFADS subjects (178 diabetic) to investigate their role in diabetes pathogenesis. We observed nominal association between four SNPs (rs10885390, rs7903146, rs12255372, and rs3814573) in three haplotype blocks and type 2 diabetes, age at diagnosis, and 2-h glucose levels (P = 0.001–0.055). Furthermore, we identified a common protective haplotype defined by these four SNPs that was significantly associated with type 2 diabetes and age at diagnosis (P = 4.2 × 10−5, relative risk [RR] 0.69; P = 6.7 × 10−6, respectively) and a haplotype that confers diabetes risk that contains the rare alleles at SNPs rs10885390 and rs12255372 (P = 0.02, RR 1.64). These data provide evidence that variation in the TCF7L2 genomic region may affect risk for type 2 diabetes in Mexican Americans, but the attributable risk may be lower than in Caucasian populations.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db06-0860
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2007
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  • 4
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    A Low-Frequency Inactivating AKT2 Variant Enriched in the Finnish Population Is Associated With Fasting Insulin Levels and Type 2 Diabetes Risk
    American Diabetes Association ; 2017
    In:  Diabetes Vol. 66, No. 7 ( 2017-07-01), p. 2019-2032
    Details
    In: Diabetes, American Diabetes Association, Vol. 66, No. 7 ( 2017-07-01), p. 2019-2032
    Abstract: To identify novel coding association signals and facilitate characterization of mechanisms influencing glycemic traits and type 2 diabetes risk, we analyzed 109,215 variants derived from exome array genotyping together with an additional 390,225 variants from exome sequence in up to 39,339 normoglycemic individuals from five ancestry groups. We identified a novel association between the coding variant (p.Pro50Thr) in AKT2 and fasting plasma insulin (FI), a gene in which rare fully penetrant mutations are causal for monogenic glycemic disorders. The low-frequency allele is associated with a 12% increase in FI levels. This variant is present at 1.1% frequency in Finns but virtually absent in individuals from other ancestries. Carriers of the FI-increasing allele had increased 2-h insulin values, decreased insulin sensitivity, and increased risk of type 2 diabetes (odds ratio 1.05). In cellular studies, the AKT2-Thr50 protein exhibited a partial loss of function. We extend the allelic spectrum for coding variants in AKT2 associated with disorders of glucose homeostasis and demonstrate bidirectional effects of variants within the pleckstrin homology domain of AKT2.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db16-1329
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2017
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  • 5
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    2093-P: Acanthosis Nigricans as a Composite Marker of Cardiometabolic Risk and Its Complex Association with Obesity and Insulin Resistance in Mexican-American Children
    American Diabetes Association ; 2019
    In:  Diabetes Vol. 68, No. Supplement_1 ( 2019-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Acanthosis nigricans (AN) is highly prevalent in Mexican Americans (MAs). It is a strong correlate of obesity, and is considered a marker of insulin resistance (IR). AN is associated with various other cardiometabolic risk factors (CMF). However, the direct causal relationship of IR with AN in obesity has been recently questioned. Therefore, we aimed to assess its genetic and environmental correlations with CMFs and examine the complex causal relationships among the troika of AN, obesity, and IR in MA, using a mediation analysis. As part of our SAFARI Study, we obtained data from 670 nondiabetic MA children, aged 6-17 years (49% girls), BMI percentile median 87 (IQR 60, 97). AN (prevalence 33%) severity scores (range 0-5) were used as a quasi-quantitative trait for analysis. We used the program SOLAR for partitioning phenotypic correlations between AN and CMFs (BMI, HOMA-IR, lipids, blood pressure, hs-C-Reactive Protein (hs-CRP), and Harvard physical fitness score (PFS)). The matrices of genetic and environmental correlations were subsequently used in mediation (direct, indirect and partial) analysis using AMOS program. We computed standardized beta values for effect measurement and goodness-of-fit indices (AIC and BCC) for model comparisons. Heritability of AN was 0.75 (p & lt;0.0001), and it was positively and significantly (p & lt;0.05) correlated with traits such as BMI, HOMA-IR, and hs-CRP, and negatively correlated with HDL-C and PFS. Of the models tested, indirect mediation analysis of BMI - & gt; HOMA-IR - & gt; AN yielded lower goodness-of-fit than a partial mediation model where BMI explained the relationship with both HOMA-IR and AN simultaneously. Using complex models, BMI was associated with AN and IR mediating most of the CMFs; but no relationship between IR and AN. In conclusion, our models suggest that obesity explains the presence of AN and IR, but no causal relationship between IR and AN in Mexican American children. Disclosure J.C. Lopez-Alvarenga: None. R. Arya: None. G. Chittoor: None. S.F. Paul: None. S.R. Puppala: None. V.S. Farook: None. S.P. Fowler: None. R.G. Resendez: None. A. Diaz-Badillo: None. D. Lehman: None. S. Mummidi: None. C. Jenkinson: None. J.L. Lynch: Board Member; Self; American Academy of Pediatrics. Consultant; Self; Novo Nordisk Inc. Research Support; Self; Daiichi Sankyo Company, Limited, National Institutes of Health, Novo Nordisk Inc., Pediatric Diabetes Consortium. R.A. DeFronzo: Advisory Panel; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Elcelyx Therapeutics, Inc., Intarcia Therapeutics, Inc., Janssen Pharmaceuticals, Inc., Novo Nordisk Inc. Research Support; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Janssen Pharmaceuticals, Inc., Merck & Co., Inc. Speaker's Bureau; Self; AstraZeneca, Novo Nordisk Inc. J. Blangero: None. D.E. Hale: None. R. Duggirala: None. Funding National Institutes of Health (R01HD049051, HD041111, DK053889, DK042273, K01DK064867, P01HL045522, DK047482, MH059490, M01-RR-01346)
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-2093-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
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  • 6
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    Genotype by Diabetes Interaction Effects on the Detection of Linkage of Glomerular Filtration Rate to a Region on Chromosome 2q in Mexican Americans
    American Diabetes Association ; 2007
    In:  Diabetes Vol. 56, No. 11 ( 2007-11-01), p. 2818-2828
    Details
    In: Diabetes, American Diabetes Association, Vol. 56, No. 11 ( 2007-11-01), p. 2818-2828
    Abstract: OBJECTIVE—Glomerular filtration rate (GFR) is used to assess the progression of renal disease. We performed linkage analysis to localize genes that influence GFR using estimated GFR data from the San Antonio Family Diabetes/Gallbladder Study. We also examined the effect of genotype by diabetes interaction (G × DM) on the detection of linkage to address whether genetic effects on GFR differ in diabetic and nondiabetic subjects. RESEARCH DESIGN AND METHODS—GFR (N = 453) was estimated using the recently recalculated Cockcroft-Gault (GFR-CGc) and the simplified Modification of Diet in Renal Disease (GFR-4VMDRD) formulae. Both estimates of GFR exhibited significant heritabilities, but only GFR-CGc showed significant G × DM interaction. We therefore performed multipoint linkage analyses on both GFR measures using models that did not include G × DM interaction effects (Model 1) and that included G × DM interaction effects (Model 2, in the case of GFR-CGc). RESULTS—The strongest evidence for linkage (Model 1) of both GFR-CGc (logarithm of odds [LOD] 2.9) and GFR-4VMDRD (LOD 2.6) occurred between markers D9S922 and D9S1120 on chromosome 9q. However, using Model 2, the strongest evidence for linkage of GFR-CGc on chromosome 2q was found near marker D2S427 (corrected LOD score [LODC] 3.3) compared with the LOD score of 2.7 based on Model 1. Potential linkages (LOD or LODC ≥1.2) were found only for GFR-CGc on chromosomes 3p, 3q, 4p, 8q, 11q, and 14q. CONCLUSIONS—We found a major locus on chromosome 2q that differentially influences GFR in diabetic and nondiabetic environments in the Mexican-American population.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db06-0984
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2007
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  • 7
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    P2 Promoter Variants of the Hepatocyte Nuclear Factor 4α Gene Are Associated With Type 2 Diabetes in Mexican Americans
    American Diabetes Association ; 2007
    In:  Diabetes Vol. 56, No. 2 ( 2007-02-01), p. 513-517
    Details
    In: Diabetes, American Diabetes Association, Vol. 56, No. 2 ( 2007-02-01), p. 513-517
    Abstract: Common and rare variants of the hepatocyte nuclear factor 4α (HNF4A) gene have been associated with type 2 diabetes and related traits in several populations suggesting the involvement of this transcription factor in diabetes pathogenesis. Single nucleotide polymorphisms (SNPs) within a large haplotype block surrounding the alternate P2 promoter, located ∼45 kb upstream from the coding region, have been investigated in several populations of varying ethnicity with inconsistent results. Additionally, SNPs located within the P1 promoter and coding region have also been inconsistently associated with type 2 diabetes. Characterization of variation across this gene region in Mexican-American populations has not been reported. We therefore examined polymorphisms across the HNF4A gene in a cohort of Mexican-American pedigrees and assessed their association with type 2 diabetes. We observed evidence for association of SNPs in the P2 promoter region with type 2 diabetes (P = 0.003) and its age at diagnosis (P = 0.003). The risk allele frequency (53%) was intermediate to that reported in Caucasian populations (20–27%) and Pima Indians (83%). No other SNPs were associated with either trait. These results support the possibility that a variant in the P2 promoter region of HNF4A, or variants in linkage disequilibrium within this region, contributes to susceptibility to type 2 diabetes in many ethnic populations including Mexican Americans.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db06-0881
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2007
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  • 8
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    A Genome-Wide Linkage Scan for Genes Controlling Variation in Renal Function Estimated by Serum Cystatin C Levels in Extended Families With Type 2 Diabetes
    American Diabetes Association ; 2006
    In:  Diabetes Vol. 55, No. 12 ( 2006-12-01), p. 3358-3365
    Details
    In: Diabetes, American Diabetes Association, Vol. 55, No. 12 ( 2006-12-01), p. 3358-3365
    Abstract: We performed a variance components linkage analysis of renal function, measured as glomerular filtration rate (GFR), in 63 extended families with multiple members with type 2 diabetes. GFR was estimated from serum concentrations of cystatin C and creatinine in 406 diabetic and 428 nondiabetic relatives. Results for cystatin C were summarized because they are superior to creatinine results. GFR aggregates in families with significant heritability (h2) in diabetic (h2 = 0.45, P & lt; 1 × 10−5) and nondiabetic (h2 = 0.36, P & lt; 1 × 10−3) relatives. Genetic correlation (rG = 0.35) between the GFR of diabetic and nondiabetic relatives was less than one (P = 0.01), suggesting that genes controlling GFR variation in these groups are different. Linkage results supported this interpretation. In diabetic relatives, linkage was strong on chromosome 2q (logarithm of odds [LOD] = 4.1) and suggestive on 10q (LOD = 3.1) and 18p (LOD = 2.2). In nondiabetic relatives, linkage was suggestive on 3q (LOD = 2.2) and 11p (LOD = 2.1). When diabetic and nondiabetic relatives were combined, strong evidence for linkage was found only on 7p (LOD = 4.0). In conclusion, partially distinct sets of genes control GFR variation in relatives with and without diabetes on chromosome 2q, possibly on 10q and 18p in the former, and on 7p in both. None of these genes overlaps with genes controlling variation in urinary albumin excretion.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db06-0781
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2006
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  • 9
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    995-P: LRG1 Mediates Diet-Induced Hyperinsulinemia by Enhancing Glucose-Stimulated Insulin Secretion
    American Diabetes Association ; 2022
    In:  Diabetes Vol. 71, No. Supplement_1 ( 2022-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 71, No. Supplement_1 ( 2022-06-01)
    Abstract: Childhood obesity and metabolic syndrome sequelae associated with early-onset insulin resistance and type 2 diabetes are at epidemic levels globally with increasing evidence for worrisome young adult health sequelae trajectories. Pediatric obesity is often associated with dramatic rise in hyperinsulinemia and acanthosis during puberty, a risk for progression to type 2 diabetes and/or hepatic steatosis. Recently, we reported leucine-rich alpha-2-glycoprotein 1 (LRG1) as an adipokine, which levels in sera are positively associated with BMI in humans. LRG1 binds with multiple metabolic organs in vivo, including the liver and pancreas. Deletion of the Lrg1 gene in mice alleviates high-fat diet (HFD) -induced hyperinsulinemia, hepatosteatosis, insulin resistance, and obesity at a young age. Our current study indicates that treating the MIN6 beta-cells with LRG1 was sufficient to trigger insulin secretion both in the absence and presence of glucose in a dose-dependent manner, specifically enhancing the first phase of insulin secretion. We also identified an LRG1 monoclonal antibody that neutralizes LRG1-related stimulation of insulin secretion in MIN6 beta-cells. Serum levels of LRG1 in young mice fed with HFD led to enhanced levels of LRG1 in sera in these mice, which preceded hyperinsulinemia and subsequent increased weight gain. Together, our results reveal that up-regulated LRG1 in circulation could be a causal factor for persistent hyperinsulinemia by directly targeting pancreatic beta-cells to enhance insulin secretion in childhood obesity and a likely biomarker for early childhood hyperinsulinemia and treatment assessments. Understanding the impact of LRG1 on childhood obesity provides critical information to prevent early-stage insulin resistance and type 2 diabetes. Disclosure D.Morales: None. J.Ryu: None. J.L.Lynch: Consultant; Novo Nordisk, Novo Nordisk, Novo Nordisk, Research Support; Beta Bionics, Inc., Beta Bionics, Inc., Beta Bionics, Inc., Jaeb Center for Health Research, Jaeb Center for Health Research, Jaeb Center for Health Research. R.Duggirala: None. L.Q.Dong: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db22-995-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
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  • 10
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    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
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.51.3.841
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2002
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