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  • 1
    Electronic Resource
    Electronic Resource
    Glucose, insulin concentrations and obesity in childhood and adolescence as predictors of NIDDM (1994)
    Springer
    Diabetologia 37 (1994), S. 617-623 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; risk factors ; glucose ; insulin ; childhood
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Metabolic abnormalities antedate the development of non-insulin-dependent diabetes mellitus (NIDDM) by some years. How these metabolic abnormalities relate to the genetic component of the disease and to the subsequent prediction of diabetes is unknown. The present study was designed to examine the association of parental diabetes with relative weight, fasting and 2-h plasma glucose and fasting and 2-h serum insulin in childhood, and to identify which of these variables were most predictive of subsequent NIDDM. Subjects comprised 1258 Pima Indians aged 5–19 years with normal glucose tolerance participating in a longitudinal population-based study. Age-sex-adjusted values of relative weight, fasting and 2-h glucose and fasting and 2-h insulin were positively associated with parental diabetes. Only one of 138 subjects with two non-diabetic parents developed diabetes. Among 1120 subjects with at least one diabetic parent, 101 (9.0%) developed diabetes during amean follow up of 8.4 years. Fastinginsulin was a significant predictor of diabetes, but did not add to the predictive value of relative weight. Relative weight and 2-h and fasting plasma glucose were the variables most predictive of NIDDM in childhood and adolescence. Against a background of parental diabetes, high fasting insulin concentrations predict diabetes, compatible with the hypothesis that insulin resistance is an early metabolic abnormality leading to NIDDM. In this study, however, its predictive power did not add significantly to that of relative weight, with which it was correlated. Both relative weight and 2-h plasma glucose in youth in those with diabetic parents are highly predictive of subsequent diabetes, and these may be the best measures currently available for identifying high-risk subjects in whom preventive measures might be targeted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403382
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Pre-diabetic blood pressure predicts urinary albumin excretion after the onset of Type 2 (non-insulin-dependent) diabetes mellitus in Pima Indians (1993)
    Springer
    Diabetologia 36 (1993), S. 998-1001 
    Details
    ISSN: 1432-0428
    Keywords: Albuminuria ; risk factors ; blood pressure ; Type 2 (non-insulin-dependent) diabetes mellitus ; Pima Indians
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Blood pressure was measured in 490 non-proteinuric Pima Indians from the Gila River Indian Community in Arizona at least 1 year before the diagnosis of Type 2 (non-insulin-dependent) diabetes mellitus. Urine albumin concentration was measured in the same subjects 0–24 years (mean 5 years) after diabetes was diagnosed. Prevalence rates of abnormal albumin excretion (albumin-to-creatinine ratio ≥100 mg/g) after the onset of Type 2 diabetes were 9%, 16%, and 23%, respectively, for the lowest to highest tertiles of pre-diabetic mean blood pressure. When controlled for age, sex, duration of diabetes and pre-diabetic 2-h post-load plasma glucose concentration, higher pre-diabetic mean blood pressure predicted abnormal urinary excretion of albumin after the onset of diabetes. This finding suggests that the higher blood pressure seen in diabetic nephropathy is not entirely a result of the renal disease, but may precede and contribute to it.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02374490
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Molecular and functional diversity of cloned cardiac potassium channels (1993)
    Springer
    Cardiovascular drugs and therapy 7 (1993), S. 585-592 
    Details
    ISSN: 1573-7241
    Keywords: K+ channel ; IT0 ; delayed rectifier ; antiarrhythmic drugs ; cardiac excitation-contraction coupling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Action potential duration is an important determinant of refractoriness in cardiac tissue and thus of the ability to propagate electrical impulses. Action potential duration is controlled in part by activation of K+ currents. Block of K+ channels and the resultant prolongation of action potential duration has become an increasingly attractive mode of anti-arrhythmic intervention. Detailed investigation of individual cardiac K+ channels has been hampered by the presence of multiple types of K+ channels in cardiac cells and the difficulty of isolating individual currents. We have approached this problem by employing a combination molecular cloning technology, heterologous channel expression systems, and biophysical analysis of expressed channels. We have focused on six different channels cloned from the rat and human cardiovascular systems. Each channel has unique functional and pharmacological characteristics, and as a group they comprise a series of mammalian K+ channel isoforms that can account for some of the diversity of channels in the mammalian heart. Each channel appears to be encoded by a different gene with little or no evidence for alternate splicing of RNA transcripts to account for the differences in primary amino acid sequence. In addition to the unique kinetic properties of these channel isoforms when expressed as homotetrameric assemblies, the formation of heterotetrameric K+ channels is also observed. The formation of heterotetrameric channels from the different gene products to create new channels with unique kinetic and pharmacological properties might further account for cardiac K+ channel diversity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00877624
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    Paper (German National Licenses)
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