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  • 1
    Electronic Resource
    Electronic Resource
    A long-term follow-up study of Japanese diabetic patients: Mortality and causes of death (1983)
    Springer
    Diabetologia 25 (1983), S. 309-312 
    Details
    ISSN: 1432-0428
    Keywords: Prognosis of diabetic patients ; long-term followup ; excess mortality ; causes of death ; vascular complications ; Japan
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A systematic 20-year follow-up study of 1,221 diabetic patients was carried out in Osaka, Japan. The mean annual mortality rates were 2.55% for men and 1.64% for women. The ratios of observed to expected numbers of deaths were 1.50 for men and 1.39 for women, indicating an excess mortality for diabetic patients of both sexes, and higher mortality in men than in women. Factors that predisposed diabetic patients to premature death were early age of onset, albuminuria, diabetic retinopathy and fasting glucose level 〉 11.1 mmol/l at the initial examination. Insulin dependence was also associated with poor prognosis. Cerebro-cardiovascular and renal diseases were the major causes of death in the diabetic patients; heart disease was the cause of death in 16.9%, cerebrovascular disease in 16.4% and renal disease in 11.9%. The relatively high incidence of renal disease as cause of death in diabetic patients was striking. Malignant neoplasms of liver and of pancreas and cirrhosis were also associated with increased ratio of observed to expected number of deaths in the patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00253191
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effect on insulin sensitivity of angiotensin converting enzyme inhibitors with or without a sulphydryl group: Bradykinin may improve insulin resistance in dogs and humans (1994)
    Springer
    Diabetologia 37 (1994), S. 300-307 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; hypertension ; angiotensin converting enzyme inhibitor ; sulphydryl group ; insulin sensitivity ; bradykinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study compared the effect on insulin sensitivity of ACE inhibitors with a sulphydryl group (captopril) or those without a sulphydryl group (delapril and enalapril) during the hyperinsulinaemic euglycaemic clamp test in both animal and clinical experiments. A possible contribution of bradykinin to the improvement of insulin sensitivity by ACE-inhibition was also studied. In healthy control and depancreatized dog experiments, administration of captopril either intravenously (3.0 mmol · kg−1) or orally (5.0 mmol · kg−1) increased insulin sensitivity indices and plasma bradykinin concentrations. In comparison, intravenous administration of an active metabolite of delapril (3.0 mmol · kg−1) and oral administration of either delapril or enalapril (5.0 mmol · kg−1) showed slight, but not significant increases in insulin sensitivity indices and plasma bradykinin concentrations. Infusion of a bradykinin antagonist (N-α-adamantaneacetyl-d-Arg-[Hyp3, Thi5,8,d-Phe7]-bradykinin) (0.5 nmol · kg−1 · min−1) abolished the effect of captopril on insulin sensitivity. Furthermore, intravenous administration of bradykinin (0.1 nmol · kg−1 · min−1) increased insulin sensitivity indices. In clinical experiments, insulin sensitivity indices decreased in the following order: normotensive healthy subjects, hypertensive non-diabetic patients, normotensive NIDDM patients and hypertensive NIDDM patients. In these four groups, oral administration of captopril (2.0 mmol · kg−1) significantly increased insulin sensitivity indices, and a concomitant increase in plasma bradykinin concentrations was observed. By contrast, oral administration of enalapril or delapril showed slight, but not significant effects on insulin sensitivity indices and plasma bradykinin concentrations. From these studies, it is concluded that ACE inhibitors with a sulphydryl group have more potent action on the improvement in insulin sensitivity than those without a sulphydryl group. Bradykinin may also possibly be involved in the mechanism underlying the improvement in insulin sensitivity associated with ACE-inhibition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00398058
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Effect on insulin sensitivity of angiotensin converting enzyme inhibitors with or without a sulphydryl group: bradykinin may improve insulin resistance in dogs and humans (1994)
    Springer
    Diabetologia 37 (1994), S. 300-307 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetes mellitus, hypertension, angiotensin converting enzyme inhibitor, sulphydryl group, insulin sensitivity, bradykinin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study compared the effect on insulin sensitivity of ACE inhibitors with a sulphydryl group (captopril) or those without a sulphydryl group (delapril and enalapril) during the hyperinsulinaemic euglycaemic clamp test in both animal and clinical experiments. A possible contribution of bradykinin to the improvement of insulin sensitivity by ACE-inhibition was also studied. In healthy control and depancreatized dog experiments, administration of captopril either intravenously (3.0 mmol·kg−1) or orally (5.0 mmol· kg−1) increased insulin sensitivity indices and plasma bradykinin concentrations. In comparison, intravenous administration of an active metabolite of delapril (3.0 mmol·kg−1) and oral administration of either delapril or enalapril (5.0 mmol·kg−1) showed slight, but not significant increases in insulin sensitivity indices and plasma bradykinin concentrations. Infusion of a bradykinin antagonist (N-α-adamantaneacetyl-D- Arg-[Hyp3,Thi5,8,D-Phe7]-bradykinin) (0.5 nmol·kg−1·min−1) abolished the effect of captopril on insulin sensitivity. Furthermore, intravenous administration of bradykinin (0.1 nmol·kg−1·min−1) increased insulin sensitivity indices. In clinical experiments, insulin sensitivity indices decreased in the following order: normotensive healthy subjects, hypertensive non-diabetic patients, normotensive NIDDM patients and hypertensive NIDDM patients. In these four groups, oral administration of captopril (2.0 mmol·kg−1) significantly increased insulin sensitivity indices, and a concomitant increase in plasma bradykinin concentrations was observed. By contrast, oral administration of enalapril or delapril showed slight, but not significant effects on insulin sensitivity indices and plasma bradykinin concentrations. From these studies, it is concluded that ACE inhibitors with a sulphydryl group have more potent action on the improvement in insulin sensitivity than those without a sulphydryl group. Bradykinin may also possibly be involved in the mechanism underlying the improvement in insulin sensitivity associated with ACE-inhibition. [Diabetologia (1994) 37: 300–307]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00398058
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Abnormal glucagon response to arginine and its normalization in obese hyperinsulinaemic patients with glucose intolerance: importance of insulin action on pancreatic Alpha cells (1991)
    Springer
    Diabetologia 34 (1991), S. 801-806 
    Details
    ISSN: 1432-0428
    Keywords: Obese hyperinsulinaemic patient ; glucagon ; Alpha cell ; insulin resistance ; arginine infusion ; artificial endocrine pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An excessive glucagon secretion to intravenous arginine infusion was found in obese hyperinsulinaemic patients with glucose intolerance. This study was designed to determine whether the glucagon hyperresponsiveness to arginine in these patients would improve by insulin infused at a high enough dose to overcome insulin resistance. By infusing high dose insulin during arginine infusion, the previously exaggerated glucagon response to arginine could be normalized. To normalize the abnormal glucagon response, insulin doses of 4.2±0.7 and 3.8±0.5 IU were required during arginine infusion in obese hyperinsulinaemic patients with impaired glucose tolerance and Type 2 (non-insulin-dependent) diabetes mellitus, respectively. This achieved plasma peak insulin levels 3 to 4 times higher than those observed in non-obese healthy subjects. Furthermore, we clarified whether or not the effect of normalizing insulin action and/or glycaemic excursions contributed to normalizing the exaggerated glucagon response to arginine in these patients. Blood glucose was clamped while high dose insulin was infused at the same levels as observed during the arginine infusion test with no insulin infusion. As a result, normalization of the exaggerated plasma glucagon response was achieved, whether hyperglycaemia existed or not. These results clearly demonstrate that, similar to non-obese hypoinsulinaemic Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients, the exaggerated Alpha-cell response to arginine infusion in obese hyperinsulinaemic patients with glucose intolerance is secondary to the reduction of insulin action on the pancreatic Alpha cell, and that the expression of insulin action plays an important part in normalizing these abnormalities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408354
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  • 5
    Electronic Resource
    Electronic Resource
    Expression of insulin receptor on clonal pancreatic alpha cells and its possible role for insulin-stimulated negative regulation of glucagon secretion (1995)
    Springer
    Diabetologia 38 (1995), S. 422-429 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic alpha cell ; In-R1-G9 ; αTC clone 6 ; insulin receptor ; glucagon secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In pancreatic alpha cells, the existence and function of the insulin receptor has not yet been fully established. In this study, to confirm the expression of functional insulin receptors in pancreatic alpha cells, we performed: 1) insulin receptor binding assay, 2) Northern blot analysis and RT-PCR (reverse transcription-polymerase chain reaction) amplification of insulin receptor mRNA, 3) immunocytochemical staining, 4) biosynthetic labelling of insulin receptor protein using [35S]methionine, 5) analysis of insulin-stimulated autophosphorylation of the insulin receptor in glucagon secreting cell lines, In-R1-G9 and αTC clone 6 cells. Glucagon secretion decreased with the addition of insulin in both cells. The receptor binding studies using [125I-Tyr-A14] insulin revealed that both cells possessed a significant number of insulin receptors (In-R1-G9: K1=2.1×109mol/l−1, K2=6.2×107 mol/l−1, R1=0.2×104, R2=1.86×104 sites/cell; αTC clone 6: K1=2.1×109 mol/l−1, K2=7.3×107 mol/l−1, R1=0.27×104, R2=1.95×104 sites/cell). Northern blot analysis as well as RT-PCR amplification showed the mRNA specific for insulin receptor in both cells. By immunocytochemical staining using anti-insulin receptor α-subunit antibody, positive immunostaining for insulin receptor was observed in both cells. [35S]Methionine labelling of both cells followed by immunoprecipitation using anti-insulin receptor antibody showed the correct size of the insulin receptor protein. The insulin receptor expressed in these cells underwent autophosphorylation by insulin stimulation. It is concluded that functional insulin receptors are properly expressed in In-R1-G9 and αTC clone 6 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410279
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Expression of insulin receptor on clonal pancreatic alpha cells and its possible role for insulin-stimulated negative regulation of glucagon secretion (1995)
    Springer
    Diabetologia 38 (1995), S. 422-429 
    Details
    ISSN: 1432-0428
    Keywords: Key words Pancreatic alpha cell ; In-R1-G9 ; αTC clone 6 ; insulin receptor ; glucagon secretion [Diabetologia (1995) 38: 422 ; 429]
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In pancreatic alpha cells, the existence and function of the insulin receptor has not yet been fully established. In this study, to confirm the expression of functional insulin receptors in pancreatic alpha cells, we performed: 1) insulin receptor binding assay, 2) Northern blot analysis and RT-PCR (reverse transcription-polymerase chain reaction) amplification of insulin receptor mRNA, 3) immunocytochemical staining, 4) biosynthetic labelling of insulin receptor protein using [35S]methionine, 5) analysis of insulin-stimulated autophosphorylation of the insulin receptor in glucagon secreting cell lines, In-R1-G9 and αTC clone 6 cells. Glucagon secretion decreased with the addition of insulin in both cells. The receptor binding studies using [125I-Tyr-A14] insulin revealed that both cells possessed a significant number of insulin receptors (In-R1-G9: K1 = 2.1 × 109 mol/l−1, K2 = 6.2 × 107 mol/l−1, R1 = 0.27 × 104, R2 = 1.86 × 104 sites/cell; αTC clone 6: K1 = 2.1 × 109 mol/l−1, K2 = 7.3 × 107 mol/l−1, R1 = 0.27 × 104, R2 = 1.95 × 104 sites/cell). Northern blot analysis as well as RT-PCR amplification showed the mRNA specific for insulin receptor in both cells. By immunocytochemical staining using anti-insulin receptor α-subunit antibody, positive immunostaining for insulin receptor was observed in both cells. [35S]Methionine labelling of both cells followed by immunoprecipitation using anti-insulin receptor antibody showed the correct size of the insulin receptor protein. The insulin receptor expressed in these cells underwent autophosphorylation by insulin stimulation. It is concluded that functional insulin receptors are properly expressed in In-R1-G9 and αTC clone 6 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410279
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Bradykinin enhances GLUT4 translocation through the increase of insulin receptor tyrosine kinase in primary adipocytes: evidence that bradykinin stimulates the insulin signalling pathway (1996)
    Springer
    Diabetologia 39 (1996), S. 412-420 
    Details
    ISSN: 1432-0428
    Keywords: Bradykinin ; bradykinin B2 receptor ; glucose uptake ; tyrosine kinase ; insulin receptor ; insulin receptor substrate-1 ; adipocyte ; GLUT4
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been suggested that bradykinin stimulates glucose uptake in experiments in vivo and in cultured cells. However, its mechanism has not yet been fully elucidated. In this study, the effects of bradykinin on the insulin signalling pathway were evaluated in isolated dog adipocytes. The bradykinin receptor binding study revealed that dog adipocytes possessed significant numbers of bradykinin receptors (Kd=83 pmol/l, binding sites = 1.7×104 site/cell). Reverse transcription-polymerase chain reaction amplification showed the mRNA specific for bradykinin B2 receptor in the adipocytes. Bradykinin alone did not increase 2-deoxyglucose uptake in adipocytes; however, in the presence of insulin (10−7 mol/l) it significantly increased 2-deoxyglucose uptake in a dose-dependent manner. Bradykinin also enhanced insulin stimulated GLUT4 translocation from the intracellular fraction to the cell membrane, and insulin induced phosphorylation of the insulin receptor Β subunit and insulin receptor substrate-1 (IRS-1) without affecting the binding affinities or numbers of cell surface insulin receptors in dog adipocytes. The time-course of insulin stimulated phosphorylation of the insulin receptor Β subunit revealed that phosphorylation reached significantly higher levels at 10 min, and stayed at the higher levels until 120 min in the presence of bradykinin, suggesting that bradykinin delayed the dephosphorylation of the insulin receptor. It is concluded that bradykinin could potentiate insulin induced glucose uptake through GLUT4 translocation. This effect could be explained by the potency of bradykinin to upregulate the insulin receptor tyrosine kinase activity which stimulates phosphorylation of IRS-1, followed by GLUT4 translocation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400672
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    Paper (German National Licenses)
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  • 8
    Electronic Resource
    Electronic Resource
    Bradykinin enhances GLUT4 translocation through the increase of insulin receptor tyrosine kinase in primary adipocytes: evidence that bradykinin stimulates the insulin signalling pathway (1996)
    Springer
    Diabetologia 39 (1996), S. 412-420 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Bradykinin ; bradykinin B2 receptor ; glucose uptake ; tyrosine kinase ; insulin receptor ; insulin receptor substrate-1 ; adipocyte ; GLUT4.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been suggested that bradykinin stimulates glucose uptake in experiments in vivo and in cultured cells. However, its mechanism has not yet been fully elucidated. In this study, the effects of bradykinin on the insulin signalling pathway were evaluated in isolated dog adipocytes. The bradykinin receptor binding study revealed that dog adipocytes possessed significant numbers of bradykinin receptors (Kd = 83 pmol/l, binding sites = 1.7 × 104 site/cell). Reverse transcription-polymerase chain reaction amplification showed the mRNA specific for bradykinin B2 receptor in the adipocytes. Bradykinin alone did not increase 2-deoxyglucose uptake in adipocytes; however, in the presence of insulin (10–7 mol/l) it significantly increased 2-deoxyglucose uptake in a dose-dependent manner. Bradykinin also enhanced insulin stimulated GLUT4 translocation from the intracellular fraction to the cell membrane, and insulin induced phosphorylation of the insulin receptor β subunit and insulin receptor substrate-1 (IRS-1) without affecting the binding affinities or numbers of cell surface insulin receptors in dog adipocytes. The time-course of insulin stimulated phosphorylation of the insulin receptor β subunit revealed that phosphorylation reached significantly higher levels at 10 min, and stayed at the higher levels until 120 min in the presence of bradykinin, suggesting that bradykinin delayed the dephosphorylation of the insulin receptor. It is concluded that bradykinin could potentiate insulin induced glucose uptake through GLUT4 translocation. This effect could be explained by the potency of bradykinin to upregulate the insulin receptor tyrosine kinase activity which stimulates phosphorylation of IRS-1, followed by GLUT4 translocation. [Diabetologia (1996) 39: 412–420]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400672
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Superconductivity in the new compound Sr"2CuO"2(CO"3)"1"-"x(BO"3)"x - The new method for carrier doping on layered copper-oxycarbonates
    Amsterdam : Elsevier
    Physica C: Superconductivity and its applications 216 (1993), S. 453-457 
    Details
    ISSN: 0921-4534
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0921-4534(93)90089-9
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  • 10
    Electronic Resource
    Electronic Resource
    New Hg based oxycarbonate superconductor HgBa"2Sr"2Cu"2O"6"+"δ(CO"3)
    Amsterdam : Elsevier
    Physica C: Superconductivity and its applications 222 (1994), S. 27-32 
    Details
    ISSN: 0921-4534
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0921-4534(94)90110-4
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