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  • 1
    Electronic Resource
    Electronic Resource
    Metabolic studies in chlorpropamide-alcohol flush positive and negative Type 2 (non-insulin dependent) diabetic patients with and without retinopathy (1983)
    Springer
    Diabetologia 24 (1983), S. 213-215 
    Details
    ISSN: 1432-0428
    Keywords: Chlorpropamide-alcohol flush ; retinopathy ; glucose tolerance test ; serum insulin ; serum triglycerides ; blood metabolites ; Type 2 diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Serum insulin and blood metabolite responses to oral glucose with and without intravenous naloxone were measured in 24 chlorpropamide-alcohol flush positive and negative Type 2 (non-insulin dependent) diabetic patients with and without retinopathy. In the chlorpropamide-alcohol flush positive patients with retinopathy, fasting blood glucose was increased 〉40% and the serum triglycerides were increased over twofold compared with each of the other three groups. Following oral glucose (50 g), the chlorpropamide-alcohol flush positive diabetic patients with complications had a lower serum insulin and higher blood glycerol than the other three groups. Thus, chlorpropamide-alcohol flush positive subjects with retinopathy showed distinct metabolic differences from the other three groups. There was no evidence that opiate-receptors influenced the metabolic response to oral glucose in the Type 2 diabetic patients since the infusion of intravenous naloxone produced no effect on the serum insulin or blood metabolites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00250165
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  • 2
    Electronic Resource
    Electronic Resource
    Tumour necrosis factor-beta polymorphism is unlikely to determine susceptibility to Type 1 (insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 576-578 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; Indian Asian ; MHC ; tumour necrosis factor ; linkage disequilibrium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tumour necrosis factor gene polymorphism has been proposed as a determinant of Type 1 (insulin-dependent) diabetes mellitus. Tumour necrosis factor-beta gene polymorphisms were analysed in 40 North Indian Asian Type 1 diabetic patients and 63 control subjects. A 5.5 kilobase gene fragment was significantly increased among the patients (82.5% vs 52%, p c〈0.01). A 10.5 kilobase fragment was significantly reduced among the patients (70% vs 90.5%, p c〈0.02). The 5.5 kilobase fragment was associated with DR3, and was not significantly increased among DR3-positive patients compared with DR3-positive control subjects. The 5.5 kilobase/5.5 kilobase genotype was increased among the diabetic subjects (30% vs 9.5%, p c〈0.03). The 10.5 kilobase/10.5 kilobase genotype was reduced among the diabetic subjects (17.5% vs 47.5%, p c〈0.02). The 5.5 kilobase/10.5 kilobase genotype was not significantly associated with disease. These findings contrast with those in a white Caucasian population, suggesting that tumour necrosis factor-beta polymorphisms do not predispose to Type 1 diabetes directly, but are in linkage disequilibrium with disease susceptibility alleles at other MHC loci.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400276
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  • 3
    Electronic Resource
    Electronic Resource
    Allele-specific gene probing supports the DQ molecule as a determinant of inherited susceptibility to Type 1 (insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 109-113 
    Details
    ISSN: 1432-0428
    Keywords: Trans-racial studies ; North Indians ; gene probing ; HLA-DQ ; Type 1 (insulin-dependent) diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Trans-racial analysis of disease associations has improved mapping of MHC-linked susceptibility to Type 1 (insulin-dependent) diabetes mellitus. In this study the contributions of the MHC class II DQA1 and DQB1 genes were investigated. Sequence-specific oligonucleotide gene probing in Type 1 diabetic and control subjects of North Indian origin supported the DQw1.18 allele of the DQB1 gene as a determinant of inherited protection against Type 1 diabetes (RR=0.12, p c〈0.05). The A3 allele of the DQA1 gene was positively associated with the disease, (RR=3.6, p c〈0.05), as was the DQw2 allele of the DQB1 gene (RR=4.6, p c〈0.01). Trans-racial comparison of these disease associations indicates that DQ alleles may directly determine an element of inherited susceptibility to Type 1 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500381
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  • 4
    Electronic Resource
    Electronic Resource
    Examination of two genetic polymorphisms within the renin-angiotensin system: no evidence for an association with nephropathy in IDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 1108-1114 
    Details
    ISSN: 1432-0428
    Keywords: Insulin-dependent diabetes mellitus ; polymerase chain reaction ; diabetic nephropathy ; angiotensinogen ; angiotensin converting enzyme ; gene polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Premature cardiovascular disease is common in insulin-dependent diabetic (IDDM) patients who develop diabetic nephropathy. Genetic polymorphism within the renin-angiotensin system has been implicated in the aetiology of a number of cardiovascular disorders; these loci are therefore candidate genes for susceptibility to diabetic renal disease. We have examined the angiotensin converting enzyme insertion/deletion polymorphism and angiotensinogen methionine 235 threonine polymorphism in a large cohort of Caucasian patients with IDDM and diabetic nephropathy. Patients were classified as having nephropathy by the presence of persistent dipstick positive proteinuria (in the absence of other causes), retinopathy and hypertension (n=242). Three groups were examined for comparison: ethnically matched non-diabetic subjects (n=187); a geographically defined cohort of newly diagnosed diabetic patients (n=341); and IDDM patients with long duration of disease (〉15 years) and no evidence of overt nephropathy (n=166). No significant difference was seen in distribution of angiotensin converting enzyme or angiotensinogen genotypes between IDDM patients with nephropathy and recently diagnosed diabetic subjects (p=0.282 and 0.584, respectively), nor the long-duration non-nephropathy diabetic subjects (p=0.701 and 0.190, respectively). We conclude that these genetic loci are unlikely to influence susceptibility to diabetic nephropathy in IDDM in the United Kingdom.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400661
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  • 5
    Electronic Resource
    Electronic Resource
    Human leucocyte antigen and insulin gene regions and nephropathy in Type I diabetes (1999)
    Springer
    Diabetologia 42 (1999), S. 1017-1020 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Type I diabetes ; diabetic nephropathy ; human leucocyte antigen ; insulin gene.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Diabetic nephropathy seems to have a strong genetic component. Genes involved in the genetic susceptibility to Type I (insulin-dependent) diabetes have been suggested to have a role in the development of diabetic nephropathy. This study aimed to examine the role of human leucocyte antigen and insulin genes in susceptibility to nephropathy in patients with Type I diabetes. Methods. We carried out a genetic association study examining insulin gene polymorphisms using three large cohorts of patients with Type I diabetes: nephropathy (n = 258), long duration non-nephropathy (n = 153) and a recently diagnosed (sporadic) diabetic cohort (n = 264). Human leucocyte antigen typing results were obtained in a smaller number due to assay failures (n = 182, 126 and 200 respectively). Results. No significant difference was seen in the distribution of human leucocyte antigen A, B, C, DR, DQA1 and DQB1 haplotypes and alleles between the three diabetic cohorts. No significant difference was seen in insulin ’ + ' and ’–' genotypes and alleles between the three diabetic cohorts. Conclusion/interpretation. Human leucocyte antigen and insulin gene loci are unlikely to have a major role in the susceptibility to nephropathy in Caucasian patients with Type I diabetes in the United Kingdom. [Diabetologia (1999) 42: 1017–1020]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051262
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  • 6
    Electronic Resource
    Electronic Resource
    Disturbed handling of ascorbic acid in diabetic patients with and without microangiopathy during high dose ascorbate supplementation (1991)
    Springer
    Diabetologia 34 (1991), S. 171-175 
    Details
    ISSN: 1432-0428
    Keywords: Ascorbic acid ; dehydroascorbic acid ; diabetes mellitus ; free radical activity ; oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Abnormalities of ascorbic acid metabolism have been reported in experimentally-induced diabetes and in diabetic patients. Ascorbate is a powerful antioxidant, a cofactor in collagen biosynthesis, and affects platelet activation, prostaglandin synthesis and the polyol pathway. This suggests a possible close interrelationship between ascorbic acid metabolism and pathways known to be influenced by diabetes. We determined serum ascorbic acid and its metabolite, dehydroascorbic acid, as indices of antioxidant status, and the ratio, dehydroascorbate/ascorbate, as an index of oxidative stress, in 20 matched diabetic patients with and 20 without microangiopathy and in 22 age-matched control subjects. Each study subject then took ascorbic acid, 1 g daily orally, for six weeks with repeat measurements taken at three and six weeks. At baseline, patients with microangiopathy had lower ascorbic acid concentrations than those without microangiopathy and control subjects (42.1±19.3 vs 55.6±20.0, p〈0.01, vs 82.9±30.9 μmol/l, p〈0.001) and elevated dehydroascorbate/ascorbate ratios (0.87±0.46 vs 0.61±0.26, p〈0.01, vs 0.38±0.14, p〈0.001). At three weeks, ascorbate concentrations rose in all groups (p〈0.0001) and was maintained in control subjects (151.5± 56.3 μmol/l), but fell in both diabetic groups by six weeks (p〈0.01). Dehydroascorbate/ascorbate ratios fell in all groups at three weeks (p〈0.0001) but rose again in the diabetic groups by six weeks (p〈0.001) and was unchanged in the control subjects. Dehydroascorbate concentrations rose significantly from baseline in all groups by six weeks of ascorbic acid supplementation (p〈0.05). No significant changes were observed in fructosamine concentrations in any group during the study. Diabetes mellitus is associated with a major disturbance of ascorbic acid metabolism which is only partially corrected by ascorbate supplementation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418271
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  • 7
    Electronic Resource
    Electronic Resource
    Identification of susceptibility loci for Type 1 (insulin-dependent) diabetes by trans-racial gene mapping (1990)
    Springer
    Diabetologia 33 (1990), S. 387-395 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 diabetes ; trans-racial studies ; DNA ; gene mapping ; HLA ; MHC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A major component of inherited susceptibility to Type 1 (insulin-dependent) diabetes mellitus has been mapped to the major histocompatibility complex. Certain gene alleles in this region determine susceptibility and resistance to the disease. Mapping of susceptibility is hindered by the limitations of conventional tissue typing techniques, and by strong linkage disequilibrium within this part of the genome. Recombinant DNA technology and trans-racial studies have been used to allow finer mapping of genetic predisposition to Type 1 diabetes. These techniques have localised alleles encoding susceptibility and resistance to the DQ region. Other alleles determining disease susceptibility remain poorly localised.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404086
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  • 8
    Electronic Resource
    Electronic Resource
    Mitochondrial gene defects in patients with NIDDM (1994)
    Springer
    Diabetologia 37 (1994), S. 372-376 
    Details
    ISSN: 1432-0428
    Keywords: Key words Genetics, diabetes mellitus, mitochondria, maternal, deafness.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Non-insulin-dependent diabetes mellitus (NIDDM) has a strong genetic component and maternal factors have recently been implicated in disease inheritance. The mitochondrial myopathies are a group of diseases which often show maternal inheritance as a result of mtDNA defects; some patients have impaired glucose tolerance. Occasional families with maternally inherited diabetes and deafness associated with a deletion or point mutation of mtDNA have been reported. To assess the importance of mitochondrial gene defects in NIDDM, 150 unrelated diabetic subjects from Wales, UK and 68 unrelated patients with diabetes and at least one affected sibling from England, UK were studied. Southern blot analysis did not show any large mtDNA deletions or duplications. One patient had a mutation in the mitochondrial tRNAleu(UUR) gene at bp 3243. This mutation is commonly associated with the syndrome of mitochondrial encephalomyopathy, lactic acidosis and stroke like episodes (MELAS). Study of this patient and his siblings showed a distinct form of late-onset diabetes associated with nerve deafness but no clinical features of the MELAS syndrome. No diabetic subject was shown to have the mtDNA mutation at position 8344 (tRNAlys) which has previously been described in the syndrome of mitochondrial encephalomyopathy and red-ragged fibres (MERRF). The role of other mitochondrial gene defects in diabetes and the pathophysiological basis of glucose intolerance in patients with the MELAS mutation requires further elucidation. [Diabetologia (1994) 37: 372–376]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408473
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  • 9
    Electronic Resource
    Electronic Resource
    Both DQA1 and DQB1 genes are implicated in HLA-associated protection from type 1 (insulin-dependent) diabetes mellitus in a British Caucasian population (1993)
    Springer
    Diabetologia 36 (1993), S. 252-257 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; HLA genes ; protection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Inherited susceptibility to Type 1 (insulin-dependent) diabetes mellitus is partly determined by HLA genes. It has been suggested that protection from disease may be conferred by HLA-DQB1 genes which encode molecules with aspartate at position 57. We investigated the contributions of HLA-DRB1, DQA1 and DQB1 genes to protection from disease. Restriction fragment length polymorphism and sequence specific oligonucleotide analysis in 156 British Caucasian Type 1 diabetic and 116 control subjects showed protection from disease was associated with DR2, DRw6 and DR7 haplotypes. The most protective DQA1 allele was DQA1*0102 which occurred on both DR2 and DRw6 haplotypes. The DQB1 alleles DQB1*0303, DQB1*0602 and DQB1*0603 were associated with protection, as was DQB1*0604, which encodes an Asp-57 negative DQβmolecule. Heterozygosity for both protective and predisposing HLA markers was reduced in diabetic compared with control subjects. We conclude that both DQA1 and DQB1 genes are implicated in HLA-associated protection from Type 1 diabetes in this British Caucasian population. The overall structure of the DQ heterodimer is critical and DQβ-Asp 57 is of secondary importance in determining protection from disease. The effect of protective HLA types may predominate over that of predisposing markers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399959
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  • 10
    Electronic Resource
    Electronic Resource
    Mitochondrial gene defects in patients with NIDDM (1994)
    Springer
    Diabetologia 37 (1994), S. 372-376 
    Details
    ISSN: 1432-0428
    Keywords: Genetics ; diabetes mellitus ; mitochondria ; maternal ; deafness
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Non-insulin-dependent diabetes mellitus (NIDDM) has a strong genetic component and maternal factors have recently been implicated in disease inheritance. The mitochondrial myopathies are a group of diseases which often show maternal inheritance as a result of mtDNA defects; some patients have impaired glucose tolerance. Occasional families with maternally inherited diabetes and deafness associated with a deletion or point mutation of mtDNA have been reported. To assess the importance of mitochondrial gene defects in NIDDM, 150 unrelated diabetic subjects from Wales, UK and 68 unrelated patients with diabetes and at least one affected sibling from England, UK were studied. Southern blot analysis did not show any large mtDNA deletions or duplications. One patient had a mutation in the mitochondrial tRNAleu(UUR) gene at bp 3243. This mutation is commonly associated with the syndrome of mitochondrial encephalomyopathy, lactic acidosis and stroke like episodes (MELAS). Study of this patient and his siblings showed a distinct form of late-onset diabetes associated with nerve deafness but no clinical features of the MELAS syndrome. No diabetic subject was shown to have the mtDNA mutation at position 8344 (tRNAlys) which has previously been described in the syndrome of mitochondrial encephalomyopathy and red-ragged fibres (MERRF). The role of other mitochondrial gene defects in diabetes and the pathophysiological basis of glucose intolerance in patients with the MELAS mutation requires further elucidation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408473
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    Paper (German National Licenses)
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