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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 17 (1979), S. 161-164 
    ISSN: 1432-0428
    Keywords: American Indians ; autoimmunity ; diabetes mellitus ; islet cell antibodies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pancreatic islet cell antibodies and 12 other autoantibodies were measured at the time of diabetes diagnosis in 46 Pima Indians, aged 17–47 years, and in 46 age-sex matched non-diabetic controls. Islet cell antibodies were found in only two diabetics, aged 20 and 25, compared with none of 46 controls. Neither of the subjects with islet cell antibodies had other autoantibodies. At least one type of autoantibody was found in 14 (30%) of the diabetics and in 14 controls, but none was significantly associated] with diabetes. This study indicates that diabetes in the Pima Indians, even those with an onset below 25 years of age, is almost entirely of type II, in that the disease is not associated with islet cell antibodies, ketoacidosis, or insulin dependence.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Key words Familial aggregation ; diabetes mellitus ; nephropathy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Both non-insulin-dependent diabetes mellitus and diabetic nephropathy show familial aggregation. If diabetes and renal disease have independent determinants (genetic or otherwise), offspring of parents with diabetic renal disease should have a similar risk of diabetes to those offspring of parents with diabetes alone. To test this hypothesis, the prevalence of diabetes was examined in a population-based pedigree study in Pima Indian offspring of three mutually exclusive parental types: 1) diabetic with renal disease, 2) diabetic, but without renal disease and 3) non-diabetic. Among offspring of one diabetic parent and one non-diabetic parent (n = 320) the prevalence of diabetes at ages 15–24 years and 25–34 years was 0 % and 11 %, respectively if the diabetic parent did not have renal disease compared with 6 % and 28 % respectively if the diabetic parent did have renal disease. Corresponding rates for offspring of two diabetic parents (n = 121) were 10 % and 17 %, respectively if neither parent had renal disease compared with 30 % and 50 %, respectively if one parent did have renal disease. The presence of renal disease in a parent with diabetes relative to diabetes alone was associated with 2.5 times the odds of diabetes (95 % confidence interval 1.4–4.3) in the offspring controlled for age, age at onset of parental diabetes and diabetes in the other parent using logistic regression. These findings provide support for parental diabetic renal disease, independent of age at onset of parental diabetes, conferring an increased risk for diabetes in the offspring. The results are compatible with the hypothesis that the susceptibility to renal disease in the parents and to diabetes in the offspring are due to shared familial environmental factors or to the same gene or set of genes. [Diabetologia (1995) 38: 221–226]
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Familial aggregation ; diabetes mellitus ; nephropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Both non-insulin-dependent diabetes mellitus and diabetic nephropathy show familial aggregation. If diabetes and renal disease have independent determinants (genetic or otherwise), offspring of parents with diabetic renal disease should have a similar risk of diabetes to those offspring of parents with diabetes alone. To test this hypothesis, the prevalence of diabetes was examined in a population-based pedigree study in Pima Indian offspring of three mutually exclusive parental types: 1) diabetic with renal disease, 2) diabetic, but without renal disease and 3) non-diabetic. Among offspring of one diabetic parent and one non-diabetic parent (n=320) the prevalence of diabetes at ages 15–24 years and 25–34 years was 0% and 11%, respectively if the diabetic parent did not have renal disease compared with 6% and 28% respectively if the diabetic parent did have renal disease. Corresponding rates for offspring of two diabetic parents (n=121) were 10% and 17%, respectively if neither parent had renal disease compared with 30% and 50%, respectively if one parent did have renal disease. The presence of renal disease in a parent with diabetes relative to diabetes alone was associated with 2.5 times the odds of diabetes (95% confidence interval 1.4–4.3) in the offspring controlled for age, age at onset of parental diabetes and diabetes in the other parent using logistic regression. These findings provide support for parental diabetic renal disease, independent of age at onset of parental diabetes, conferring an increased risk for diabetes in the offspring. The results are compatible with the hypothesis that the susceptibility to renal disease in the parents and to diabetes in the offspring are due to shared familial environmental factors or to the same gene or set of genes.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Impaired glucose tolerance ; diabetes mellitus ; prevalence ; Melanesian ; Polynesian ; glucose tolerance ; genetics ; environment ; rural ; urban
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The study of different ethnic groups living in the same physical environment provides the opportunity to examine interaction of genetic and environmental factors in the aetiology of diabetes mellitus. In rural New Caledonia, the prevalence of diabetes was higher in part-Polynesians than in Melanesians: males — 6.6 versus 0.5%; females — 6.3 versus 3.5% respectively. The prevalence of abnormal glucose tolerance (impaired glucose tolerance and diabetes) was 11.5 and 15.7% in part-Polynesian males and females, respectively, and 4.7 and 9.2% in Melanesian males and females. Mean age and degree of obesity in these ethnic groups were sufficiently similar to suggest that these factors played no significant role in the difference in diabetes prevalence. Furthermore, adjustment of relative risk of impaired glucose tolerance and diabetes for age and obesity indicated that the modest differences between groups were not responsible for the observed variation in diabetes prevalence. The differences in prevalence of impaired glucose tolerance and diabetes between Melanesians and part-Polynesians may be genetically determined, although the role of certain environmental factors other than obesity, e.g. differences in physical activity or qualitative aspects of diet, cannot be excluded.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Pima Indians ; diabetes mellitus ; pancreatic islets ; islet amyloid ; islet amyloid polypeptide ; insulin resistance ; glucose tolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid may have a pathological role in the development of Type 2 (non-insulin-dependent) diabetes mellitus. The prevalence of islet amyloid has been investigated on post-mortem pancreatic tissue from both diabetic and non-diabetic Pima Indian subjects who had previously been assessed by oral glucose tolerance tests. Islets were examined for amyloid deposits and for cellular immunoreactivity to pancreatic hormones and islet amyloid polypeptide, the constituent peptide of islet amyloid. Twenty of 26 diabetic subjects (77%) had islet amyloid, compared with one of 14 non-diabetic subjects (7%). Twelve of the diabetic subjects (46%) had amyloid in more than 10% of their islets, whereas only 4% of islets were affected in a single non-diabetic subject. Positive immunoreactivity for islet amyloid peptide was present in the islet amyloid and in islet cells in 54% of the diabetic and 50% of the non-diabetic subjects. Islet amyloid in diabetic Pima Indians may indicate a primary Beta-cell defect which interacts with insulin resistance to produce diabetes, or may develop as a result of Beta-cell dysfunction induced by insulin resistance and hyperglycaemia.
    Type of Medium: Electronic Resource
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