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  • Keywords Insulin-dependent diabetes mellitus  (3)
  • Insulin receptor gene  (1)
  • 1
    Digitale Medien
    Digitale Medien
    Molecular methods for the study of the genetic determinants of nephropathy in type 1 (insulin-dependent) diabetes (1992)
    Springer
    Acta diabetologica 29 (1992), S. 136-141 
    Details
    ISSN: 1432-5233
    Schlagwort(e): Angiotensinogen gene ; Insulin receptor gene ; Methods of molecular genetics ; Nephropathy in type 1 (insulin-dependent) diabetes
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Recently, evidence has accumulated that genetic factors may contribute to the development of diabetic nephropathy in patients with type 1 (insulin-dependent) diabetes mellitus. To identify variation at a gene locus, newly developed methods are introduced which employ denaturing gradient gel electrophoresis (DGGE) to study sequence differences in polymerase chain reaction (PCR)-amplified DNA fragments as well as in genomic DNA. These techniques are illustrated with studies of the angiotensinogen gene and the insulin receptor gene. In preliminary data from a comparison between individuals with and without diabetic nephropathy, we found no DNA sequence difference in the part of the angiotensinogen gene coding for angiotensin I. We did find, however, different distributions of a DNA polymorphism detected with the probe corresponding to exons 7 and 8 of the insulin receptor gene inRsaI DGGE blots in a comparison of patients with slow and fast progressing nephropathy. The interpretation of this finding and the need for further studies are discussed. In conclusion, the advent of methods of molecular genetics makes possible studies on genetic determinants of diabetic nephropathy. However, more clinical and epidemiological data are needed to find out how many genes are involved and how they interact with exposure to diabetes. Foremost, DNA from families with two or more siblings with diabetic nephropathy must be collected so that genetic studies will be possible.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00573478
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  • 2
    Digitale Medien
    Digitale Medien
    Diabetes susceptibility at IDDM2 cannot be positively mapped to the VNTR locus of the insulin gene (1996)
    Springer
    Diabetologia 39 (1996), S. 594-599 
    Details
    ISSN: 1432-0428
    Schlagwort(e): Keywords Insulin-dependent diabetes mellitus ; insulin gene ; tyrosine hydroxylase gene ; VNTR ; linkage disequilibrium.
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary An inconsistency has come to light between the conclusion of Lucassen et al. that IDDM2 (11p15.5) must lie within a 4.1 kilobase (kb) segment at the insulin (INS) locus and their own data showing statistically significant associations between insulin-dependent diabetes mellitus (IDDM) and markers beyond the boundaries of that segment. We present data from an independent study of 201 IDDM patients and 107 non-diabetic control subjects that also show significant association with a marker 5 ′ of the INS locus. Patients and control subjects were genotyped at INS/ + 1140 A/C (a surrogate for the variable number tandem repeat (VNTR) polymorphism in the regulatory part of the INS gene) and a marker 5 ′ of the tyrosine hydroxylase (TH) gene, TH/pINS500RsaI, making it 10 kb 5 ′ of the VNTR. Homozygotes for INS/ + 1140 allele ’ + ' were significantly more frequent among IDDM patients than among control subjects (73 vs 45 %, p 〈 0.001) giving an odds ratio of 3.3 (95 % confidence interval (CI): 2.0–5.3). A very similar association was found for homozygotes for the TH/RsaI allele ’ + ' (53 vs 31 %, p 〈 0.001) giving an odds ratio of 2.6 (95 %CI 1.6–4.2). By multilocus analysis, the TH/RsaI allele ’ + ' identified a subset of INS/ + 1140 alleles ’ + ' haplotypes that are more specifically associated with IDDM (odds ratio = 5.4, 95 %CI 2.9–10.4) than allele + 1140 ’ + ' as a whole. In conclusion, the segment of chromosome 11 that is associated with IDDM spans, at least, the INS and TH loci. No legitimate claim can be made that IDDM2 corresponds to the VNTR polymorphism at the INS locus until the correct boundaries for IDDM2 have been defined and other loci within them have been excluded as determinants of IDDM. [Diabetologia (1996) 39: 594–599]
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00403307
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  • 3
    Digitale Medien
    Digitale Medien
    Synergistic effect of angiotensin II type 1 receptor genotype and poor glycaemic control on risk of nephropathy in IDDM (1997)
    Springer
    Diabetologia 40 (1997), S. 1293-1299 
    Details
    ISSN: 1432-0428
    Schlagwort(e): Keywords Insulin-dependent diabetes mellitus ; diabetic nephropathy ; angiotensin II receptor ; DNA polymorphisms ; genetics.
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary We investigated the contribution of polymorphisms in the angiotensin II type 1 receptor gene (AGTR1) to renal complications in an inception cohort of 152 insulin-dependent diabetic (IDDM) patients examined 15–21 years after diabetes onset. This nested case-control study included 79 normoalbuminuric control subjects and 73 cases with evidence of nephropathy ranging from microalbuminuria to overt proteinuria. Subjects were genotyped for two AGTR1 polymorphisms (T573→C and A1166→C), and an adjacent CA repeat microsatellite. Allele C1166 and the 140 bp allele of the microsatellite were more frequent among nephropathy cases than normoalbuminuric control subjects (0.322 vs 0.247, and 0.618 vs 0.521, respectively), but these differences were not statistically significant. Although not significant by themselves, the AGTR1 polymorphisms contributed significantly to the risk of diabetic nephropathy when accompanied by poor glycaemic control. Among patients with frequent severe hyperglycaemia during the first decade of diabetes, the relative risk of nephropathy among allele C1166 carriers was 12.1 (95 % CI: 3.7–39.8), whereas it was only 1.4 (95 % CI: 0.6–3.5) among allele A1166 homozygotes. The difference between relative risks was highly significant (χ 2 = 8.25, p = 0.004 with 1 df). A similar pattern of higher risk of microalbuminuria, specifically among those carriers of allele C1166 who had poor glycaemic control was also found in an independent study of a cross-sectional sample of 551 IDDM individuals, although the effect was smaller in magnitude. We conclude that DNA sequence differences in the AGTR1 gene may modify the noxious effects of hyperglycaemia on the kidney. Allele C1166 carriers might especially benefit from nephropathy prevention programmes. [Diabetologia (1997) 40: 1293–1299]
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s001250050823
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  • 4
    Digitale Medien
    Digitale Medien
    Familial factors determine the development of diabetic nephropathy in patients with IDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 940-945 
    Details
    ISSN: 1432-0428
    Schlagwort(e): Keywords Insulin-dependent diabetes mellitus ; genetics of diabetic nephropathy ; family studies.
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary To evaluate familial factors in the development of diabetic nephropathy in insulin-dependent diabetes mellitus (IDDM) we examined concordance for diabetic nephropathy in families with multiple IDDM siblings. Families (n = 110) were identified through Joslin Clinic patients (probands) with a sibling having IDDM. To be eligible, the probands' and siblings' ages at IDDM diagnosis were less than 21 years, and IDDM duration was more than 15 years for probands and more than 10 years for siblings. Mean post-pubertal diabetes duration was 23 years for probands (n = 110) and 21 years for siblings (n = 125). Nephropathy history was determined by medical record review for deceased patients and those with persistent proteinuria or end-stage renal disease to ascertain the date of onset of persistent proteinuria. For patients without documented nephropathy, the albumin/creatinine ratio was measured in multiple urine samples. The cumulative incidence of persistent proteinuria according to post-pubertal duration of IDDM was determined by life-table analysis. For probands and siblings combined, the cumulative incidence of advanced diabetic nephropathy after 30 years of IDDM was 35 %, but the risk in siblings varied according to the proband's renal status. The cumulative risk in siblings after 25 years of IDDM (post-puberty) was 71.5 % if the proband had persistent proteinuria but only 25.4 % if the proband did not (p 〈 0.001). A difference of nearly 50 % in the risk to IDDM siblings, depending upon the IDDM proband's renal status, is consistent with a major gene effect that predisposes an individual with IDDM to develop advanced diabetic nephropathy. [Diabetologia (1996) 39: 940–945]
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00403913
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