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  • 1
    Electronic Resource
    Electronic Resource
    Temperature-dependent regulation of d-cis-[^3H]diltiazem binding to Ca^2^+ channels by 1,4-dihydropyridine channel agonists and antagonists
    Amsterdam : Elsevier
    FEBS Letters 160 (1983), S. 226-232 
    Details
    ISSN: 0014-5793
    Keywords: 1,4-Dihydropyridine ; Ca^2^+-channel ; Skeletal muscle ; d-cis-[^3H]-diltiazem
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0014-5793(83)80972-7
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Spontaneous glucose intolerance in the progeny of low dose streptozotocin-induced diabetic mice (1993)
    Springer
    Diabetologia 36 (1993), S. 1245-1251 
    Details
    ISSN: 1432-0428
    Keywords: Streptozotocin ; offspring ; insulitis ; islet perifusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Multiple low doses of streptozotocin (LDS) induce low-incidence diabetes mellitus in Balb/cHan and high-incidence diabetes in CD-1 mice. We studied offspring of diabetic parents in both strains. Group 1 consisted of litters from control mice with no streptozotocin treatment. Group 2 litters had an LDS diabetic mother and a control father, group 3 litters had control mother with LDS diabetic father, and group 4 litters had both, LDS diabetic mother and father. Diabetes was induced by 5×40 mg streptozotocin per kg on five consecutive days. Progeny of diabetic mothers showed a state of reduced glucose tolerance associated with reduced glucose disappearance during intravenous glucose tolerance test and increased insulin secretion of isolated islets of Langerhans. These metabolic abnormalities predominated in the male litters of both strains of mice. Amniotic insulin was increased in diabetic mothers during pregnancy. No histologic abnormalities were observed in group 2 progeny. Pancreases in male offspring of LDS diabetic CD-1 fathers (group 3) were studied for insulitis. Insulitis was found in 40% of mice with normal glucose tolerance. A single subdiabetogenic dose of streptozotocin (40 mg/kg) induced insulitis in 90% of pancreases accompanied by reduced insulin release of isolated islets. By contrast, male Balb/cHan progeny of diabetic fathers failed to develop insulitis. In conclusion, we found (1) parental LDS diabetes was transmitted more often to male offspring, (2) maternal LDS diabetes was associated with hyperinsulin secretion and glucose intolerance in the offspring and (3) paternal LDS diabetes was accompanied by insulitis and insulin secretion deficiency in CD-1 progeny.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400801
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Glucagon-like-peptide-1 (7–36) amide improves glucose sensitivity in beta-cells of NOD mice (1996)
    Springer
    Acta diabetologica 33 (1996), S. 19-24 
    Details
    ISSN: 1432-5233
    Keywords: Key words  Glucagon-like-peptide-1 ; Prediabetes ; NOD mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract   The effect of the insulinotropic gut hormone glucagon-like-peptide-1 (GLP-1) was studied on the residual insulin capacity of prediabetic nonobese diabetic (NOD) mice, a model of insulin-dependent diabetes mellitus (type 1). This was done using isolated pancreas perfusion and dynamic islet perifusion. Prediabetes was defined by insulitis and fasting normoglycemia. Insulitis occurred in 100% of NOD mice beyond the age of 12 weeks. K values in the intravenous glucose tolerance test were reduced in 20-week-old NOD mice compared with age-matched non-diabetes-prone NOR (nonobese resistant) mice (2.4±1.1 vs 3.8±1.5% min–1, P〈0.05). Prediabetic NOD pancreases were characterized by a complete loss of the glucose-induced first-phase insulin release. In perifused NOD islets GLP-1, at concentrations already effective in normal islets, left the insulin release unaltered. However, a significant rise of glucose-dependent insulin secretion occurred for GLP-1 concentrations 〉0.1 nM. This was obtained with both techniques, dynamic islet perifusion and isolated pancreas perfusion, indicating a direct effect of GLP-1 on the beta-cell. Analysis of glucose-insulin dose-response curves revealed a marked improvement of glucose sensitivity of the NOD endocrine pancreas in the presence of GLP-1 (half-maximal insulin output without GLP-1 15.2 mM and with GLP-1 9.4 mM, P〈0.002). We conclude that GLP-1 can successfully reverse the glucose sensing defect of islets affected by insulitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571935
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Glucagon-like-peptide-1 (7–36) amide improves glucose sensitivity in beta-cells of NOD mice (1996)
    Springer
    Acta diabetologica 33 (1996), S. 19-24 
    Details
    ISSN: 1432-5233
    Keywords: Glucagon-like-peptide-1 ; Prediabetes ; NOD mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of the insulinotropic gut hormone glucagon-like-peptide-1 (GLP-1) was studied on the residual insulin capacity of prediabetic nonobese diabetic (NOD) mice, a model of insulin-dependent diabetes mellitus (type 1). This was done using isolated pancreas perfusion and dynamic islet perifusion. Prediabetes was defined by insulitis and fasting normoglycemia. Insultis occurred in 100% of NOD mice beyond the age of 12 weeks. K values in the intravenous glucose tolerance test were reduced in 20-week-old NOD mice compared with agematched non-diabetes-prone NOR (nonobese resistant) mice (2.4±1.1 vs 3.8±1.5% min−1,P〈0.05). Prediabetic NOD pancreases were characterized by a complete loss of the glucose-induced first-phase insulin release. In perifused NOD islets GLP-1, at concentrations already effective in normal islets, left the insulin release unaltered. However, a significant rise of glucose-dependent insulin secretion occurred for GLP-1 concentrations〉0.1 nM. This was obtained with both techniques, dynamic islet perifusion and isolated pancreas perfusion, indicating a direct effect of GLP-1 on the beta-cell. Analysis of glucose-insulin dose-response curves revealed a marked improvement of glucose sensitivity of the NOD endocrine pancreas in the presence of GLP-1 (half-maximal insulin output without GLP-1 15.2 mM and with GLP-1 9.4 mM,P〈0.002). We conclude that GLP-1 can successfully reverse the glucose sensing defect of islets affected by insulitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571935
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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