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  • 1
    Electronic Resource
    Electronic Resource
    Mortality from cardiovascular diseases among diabetics (1977)
    Springer
    Diabetologia 13 (1977), S. 345-350 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; mortality ; coronary heart disease ; cerebrovascular disease ; hypoglycaemic therapy ; cohort studies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A retrospective analysis of a cohort of 5210 diabetic patients revealed a mortality rate 1.3 times higher than in the general population of Warsaw. The higher death rate in the cohort under study was mainly due to an excess mortality from coronary heart disease and cerebrovascular disease. The excess mortality was greater in men than in women. The risk of death from cardiovascular diseases was higher among the patients with early onset diabetes. Mortality from cerebrovascular disease was highest in patients treated with insulin, intermediate in the group treated with oral drugs, and lowest in the group treated only with diet. The mortality ratio from coronary heart disease in men was not related to the method of hypoglycaemic therapy given at the onset or during the course of the diabetes. In women, the highest mortality was in the group treated with insulin, intermediate in the group treated with oral agents, and lowest in the group treated with diet only.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01223277
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  • 2
    Electronic Resource
    Electronic Resource
    Interrelationships of microangiopathy, plasma glucose and other risk factors in 3583 diabetic patients: A multinational study (1982)
    Springer
    Diabetologia 22 (1982), S. 412-420 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes ; retinopathy ; glomerulosclerosis ; microangiopathy ; plasma glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a multinational study, fasting plasma glucose values in 3583 diabetic patients, aged 34–56 years, were related to the characteristics of these subjects and to the presence and severity of microangiopathy as ascertained by standardised methods. The patients were from nine different populations and ranged in number from 193 to 686 per population (London, Warsaw, Berlin (FRG), New Delhi, Tokyo, Havana, Oklahoma Indians, Arizona Pima Indians, and a national sample in Switzerland). In the total group, mean fasting plasma glucose was 8.1 mmol/l for those on diet alone, 9.7 mmol/l for those on oral agents, and 12.7 mmol/l for insulin-treated patients, of whom 25% had values exceeding 16.5 mmol/l. Since many variables were measured in each patient, it was possible to take into account many confounding factors in evaluating the relationship of plasma glucose levels to retinopathy and nephropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00282582
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  • 3
    Electronic Resource
    Electronic Resource
    Prevalence of diabetes mellitus, coronary heart disease and hypertension in the families of insulin dependent and insulin independent diabetics (1981)
    Springer
    Diabetologia 21 (1981), S. 520-524 
    Details
    ISSN: 1432-0428
    Keywords: Insulin dependent diabetes ; insulin independent diabetes ; familial occurrence of diabetes mellitus ; familial occurrence of coronary heart disease ; familial occurrence of hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary During an epidemiological study concerning the fate of diabetics in Warsaw, 2,356 subjects (aged 35–68 years with duration of diabetes mellitus of 3–11 years) were investigated with particular relevance to the presence of diabetes mellitus, coronary heart disease, and hypertension in their parents and siblings. Diabetics were classified into the following groups: insulin dependent, insulin independent nonobese, insulin independent obese, and a group in whom the distinction between insulin dependence and insulin independence was unclear. The findings in these groups were compared with the frequencies of these diseases in a random sample of the general population. There was an excess of diabetes in close relatives of all the diabetic groups. This was highest for insulin independent non-obese diabetics. There was no difference in the prevalence of coronary heart disease and hypertension in close relatives of insulin dependent diabetics when compared with the general population, but these were twice as prevalent in close relatives of the insulin independent non-obese group. Obese insulin independent diabetics reported a similar excess of coronary heart disease and hypertension in siblings, but the excess was less marked in parents. The prevalence of these diseases in families of probands with unclassified diabetes was intermediate between the other two groups. These results demonstrate an aggregation of diabetes mellitus with coronary heart disease and hypertension in families of insulin independent non-obese diabetics. This provides further evidence for heterogeneity in diabetes mellitus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00281541
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  • 4
    Electronic Resource
    Electronic Resource
    Familial factors determine the development of diabetic nephropathy in patients with IDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 940-945 
    Details
    ISSN: 1432-0428
    Keywords: Insulin-dependent diabetes mellitus ; genetics of diabetic nephropathy ; family studies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403913
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  • 5
    Electronic Resource
    Electronic Resource
    The C825T polymorphism in the human G-protein β3 subunit gene is not associated with diabetic nephropathy in Type I diabetes mellitus (1998)
    Springer
    Diabetologia 41 (1998), S. 1304-1308 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic ; nephropathy ; susceptibility ; GNB3 ; hypertension ; Type I diabetes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In Type I (insulin-dependent) diabetes mellitus a genetic predisposition exists to nephropathy and is related to parental hypertension. Enhanced G-protein activation, a cellular phenotype observed in cultured cells from patients with essential hypertension, was recently documented in Type I diabetic subjects with nephropathy. This enhanced G-protein activation has been associated with a genetic variant in the G-protein β3 subunit, GNB3. A C→T polymorphism at position 825 in exon 10 is associated with G-protein activation, the T allele associated with enhanced activity. Furthermore the T allele was observed more frequently in a group with essential hypertension. In this report we have analysed the role of the C825T polymorphism in the predisposition to diabetic nephropathy in Type I diabetes. We have investigated the frequency of this polymorphism in a large case-control study and found no association of the T allele with diabetic nephropathy. Specifically carriage of the T allele as CT or TT was observed in 49 % of 200 Type I diabetic control subjects with normoalbuminuria (diabetes duration 24 years) compared with 53 % of 216 Type I diabetic subjects with nephropathy (overt proteinuria or end-stage renal failure). Within this group we have also examined the inheritance of C825T alleles in a family study and found no evidence for excess transmission of the T allele to Type I diabetic offspring with nephropathy (T allele transmitted to 51 % of nephropathy offspring, C allele transmitted to 49 % of nephropathy offspring, p = 0.79). In none of the Type I diabetic datasets examined was there any effect of genotype on variation in systolic or diastolic blood pressure. In conclusion we can find no evidence for the C825T polymorphism of the β3 G-protein subunit as a major gene in the susceptibility to diabetic nephropathy in Type I diabetes. [Diabetologia (1998) 41: 1304–1308]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051069
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  • 6
    Electronic Resource
    Electronic Resource
    Familial factors determine the development of diabetic nephropathy in patients with IDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 940-945 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin-dependent diabetes mellitus ; genetics of diabetic nephropathy ; family studies.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403913
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  • 7
    Electronic Resource
    Electronic Resource
    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
    Keywords: Keywords Insulin-dependent diabetes mellitus ; diabetic nephropathy ; angiotensin II receptor ; DNA polymorphisms ; genetics.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050823
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  • 8
    Electronic Resource
    Electronic Resource
    Polymorphisms of human paraoxonase 1 gene (PON1) and susceptibility to diabetic nephropathy in Type I diabetes mellitus (2000)
    Springer
    Diabetologia 43 (2000), S. 1540-1543 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; PON1 ; polymorphism ; case-control study ; Type I diabetes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Oxidative stress is a putative mechanism in the development of diabetic nephropathy. Paraoxonase gene 1 is an HDL-bound enzyme that protects tissues against oxidative damage. Three common polymorphisms of paraoxonase gene 1, T-107C in the promoter, Leu54Met and Gln192Arg, that modify paraoxonase activity have been associated with cardiovascular disease. This study aimed to find whether these polymorphisms also contribute to the development of diabetic nephropathy. Methods. The association between diabetic nephropathy and these three polymorphisms was examined in a case-control study. For this purpose, genomic DNA was collected from 188 patients with Type I (insulin-dependent) diabetes mellitus and diabetic nephropathy and from 179 unrelated patients with Type I diabetes but without diabetic nephropathy despite the duration of diabetes of 15 or more years. Results. The genotype and allele frequencies for each of the three polymorphisms (T-107C, Leu54Met and Gln192Arg) were similar in cases and control subjects. Conclusion/interpretation. The three polymorphisms in paraoxonase gene 1 that have been associated with serum levels of paraoxonase are not associated with diabetic nephropathy. We show that this genetically determined component of the antioxidant capacity of HDL does not play a critical part in the development of diabetic nephropathy. [Diabetologia (2000) 43: 1540–1543]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051566
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  • 9
    Electronic Resource
    Electronic Resource
    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
    Keywords: Keywords Insulin-dependent diabetes mellitus ; insulin gene ; tyrosine hydroxylase gene ; VNTR ; linkage disequilibrium.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403307
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  • 10
    Electronic Resource
    Electronic Resource
    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
    Keywords: Insulin-dependent diabetes mellitus ; insulin gene ; tyrosine hydroxylase gene ; VNTR ; linkage disequilibrium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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/pINS500-RsaI, 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/RsaIallele ‘+’ (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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403307
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