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  • 1
    Electronic Resource
    Electronic Resource
    Non-parallelism of islet amyloid polypeptide (amylin) and insulin gene expression in rat islets following dexamethasone treatment (1995)
    Springer
    Diabetologia 38 (1995), S. 395-402 
    Details
    ISSN: 1432-0428
    Keywords: Key words Islet amyloid polypeptide ; amylin ; insulin ; dexamethasone ; rat ; pancreatic islets ; in situ hybridization ; gene expression ; mRNA.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide (IAPP), a novel islet hormone candidate, has been reported to be over-expressed relative to insulin in rats following dexamethasone treatment. In order to investigate the expression of IAPP and insulin following dexamethasone treatment of rats for 12 days, we applied in situ hybridization and immunocytochemistry, allowing us to evaluate islet changes in gene expression and morphology. Tissue concentrations of IAPP and insulin were measured by radioimmunoassay. A low dose of dexamethasone (0.2 mg/kg daily) increased the islet levels of IAPP and insulin mRNA to 249 ± 13 % and 150 ± 24 % of controls, respectively (p 〈 0.001 and p 〈 0.01). A high dose of dexamethasone (2.0 mg/kg daily) increased the islet levels of IAPP and insulin mRNA to 490 ± 13 % and 203 ± 9 % of controls, respectively (p 〈 0.001 and p 〈 0.001). The pancreatic concentration of IAPP increased more than that of insulin (p 〈 0.05). Morphometric analysis revealed that dexamethasone treatment induced both hyperplasia and hypertrophy of insulin cells. Changes in the cellular localization of IAPP and insulin mRNA were not observed. Thus, we conclude that the increased level of IAPP mRNA is due to both an increase at the cellular level as well as hyperplasia/hypertrophy of insulin cells. In contrast, the increased level of insulin mRNA appears to be due to hyperplasia/hypertrophy of insulin cells, since insulin gene expression decreased at the cellular level (p 〈 0.001 vs controls). These observations provide further evidence that IAPP and insulin gene expression are regulated in a non-parallel fashion, which may be relevant to the pathogenesis of non-insulin-dependent diabetes mellitus [Diabetologia (1995) 38: 395–402]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410276
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  • 2
    Electronic Resource
    Electronic Resource
    Islet amyloid polypeptide (amylin) and insulin are differentially expressed in chronic diabetes induced by streptozotocin in rats (1996)
    Springer
    Diabetologia 39 (1996), S. 1004-1004 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403926
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Non-parallelism of islet amyloid polypeptide (amylin) and insulin gene expression in rat islets following dexamethasone treatment (1995)
    Springer
    Diabetologia 38 (1995), S. 395-402 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide ; amylin ; insulin ; dexamethasone ; rat ; pancreatic islets ; in situ hybridization ; gene expression ; mRNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide (IAPP), a novel islet hormone candidate, has been reported to be over-expressed relative to insulin in rats following dexamethasone treatment. In order to investigate the expression of IAPP and insulin following dexamethasone treatment of rats for 12 days, we applied in situ hybridization and immunocytochemistry, allowing us to evaluate islet changes in gene expression and morphology. Tissue concentrations of IAPP and insulin were measured by radioimmunoassay. A low dose of dexamethasone (0.2 mg/kg daily) increased the islet levels of IAPP and insulin mRNA to 249±13% and 150±24% of controls, respectively (p〈0.001 and p〈0.01). A high dose of dexamethasone (2.0 mg/kg daily) increased the islet levels of IAPP and insulin mRNA to 490±13% and 203±9% of controls, respectively (p〈0.001 and p〈0.001). The pancreatic concentration of IAPP increased more than that of insulin (p〈0.05). Morphometric analysis revealed that dexamethasone treatment induced both hyperplasia and hypertrophy of insulin cells. Changes in the cellular localization of IAPP and insulin mRNA were not observed. Thus, we conclude that the increased level of IAPP mRNA is due to both an increase at the cellular level as well as hyperplasia/hypertrophy of insulin cells. In contrast, the increased level of insulin mRNA appears to be due to hyperplasia/hypertrophy of insulin cells, since insulin gene expression decreased at the cellular level (p〈0.001 vs controls). These observations provide further evidence that IAPP and insulin gene expression are regulated in a non-parallel fashion, which may be relevant to the pathogenesis of non-insulin-dependent diabetes mellitus
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410276
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Islet amyloid polypeptide (amylin) and insulin are differentially expressed in chronic diabetes induced by streptozotocin in rats (1996)
    Springer
    Diabetologia 39 (1996), S. 649-657 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide (IAPP) ; amylin ; insulin ; messenger RNA (mRNA) ; in situ hybridization ; streptozotocin ; dexamethasone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide (IAPP) is over-expressed relative to insulin under several experimental conditions relevant to diabetes mellitus, including the immediate phase (7 days) following induction of streptozotocin diabetes. In the present study, IAPP and insulin gene expression were examined in chronic streptozotocin diabetes (3 weeks) in rats. Quantitative in situ hybridization, determining grain areas and optical densities of mRNA labelling, revealed that IAPP and insulin expression were reduced at the islet level at both low and high streptozotocin doses, partly due to reduced beta-cell mass. In contrast, the cellular levels of IAPP mRNA were either increased or unaffected at the low and high streptozotocin doses, respectively, whereas those of insulin mRNA were unaffected or reduced. When dexamethasone was administered to rats given the low streptozotocin dose, IAPP expression was increased, whereas that of insulin was markedly reduced. Immunocytochemistry revealed that IAPP predominantly occurred in insulin cells and to a lesser extent in somatostatin cells at all treatments examined. Our findings demonstrate that IAPP and insulin gene expression are differentially regulated; the over-expression of IAPP relative to insulin is augmented when the beta-cell insult is aggravated, in our experiments represented by massive beta-cell destruction (high streptozotocin dose) or a combination of moderate beta-cell damage and peripheral insulin resistance (low streptozotocin dose and dexamethasone). An over-expression of IAPP relative to insulin may therefore be involved in diabetes pathogenesis, contributing to its metabolic perturbations, possibly through the capacity of IAPP to restrain insulin release and action and to form islet amyloid.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418536
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Islet amyloid polypeptide (amylin) and insulin are differentially expressed in chronic diabetes induced by streptozotocin in rats (1996)
    Springer
    Diabetologia 39 (1996), S. 649-657 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Islet amyloid polypeptide (IAPP) ; amylin ; insulin ; messenger RNA (mRNA) ; in situ hybridization ; streptozotocin ; dexamethasone.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide (IAPP) is over-expressed relative to insulin under several experimental conditions relevant to diabetes mellitus, including the immediate phase (7 days) following induction of streptozotocin diabetes. In the present study, IAPP and insulin gene expression were examined in chronic streptozotocin diabetes (3 weeks) in rats. Quantitative in situ hybridization, determining grain areas and optical densities of mRNA labelling, revealed that IAPP and insulin expression were reduced at the islet level at both low and high streptozotocin doses, partly due to reduced beta-cell mass. In contrast, the cellular levels of IAPP mRNA were either increased or unaffected at the low and high streptozotocin doses, respectively, whereas those of insulin mRNA were unaffected or reduced. When dexamethasone was administered to rats given the low streptozotocin dose, IAPP expression was increased, whereas that of insulin was markedly reduced. Immunocytochemistry revealed that IAPP predominantly occurred in insulin cells and to a lesser extent in somatostatin cells at all treatments examined. Our findings demonstrate that IAPP and insulin gene expression are differentially regulated; the over-expression of IAPP relative to insulin is augmented when the beta-cell insult is aggravated, in our experiments represented by massive beta-cell destruction (high streptozotocin dose) or a combination of moderate beta-cell damage and peripheral insulin resistance (low streptozotocin dose and dexamethasone). An over-expression of IAPP relative to insulin may therefore be involved in diabetes pathogenesis, contributing to its metabolic perturbations, possibly through the capacity of IAPP to restrain insulin release and action and to form islet amyloid. [Diabetologia (1996) 39: 649–657]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050492
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  • 6
    Electronic Resource
    Electronic Resource
    Blockade of muscarinic transmission increases the frequency of diabetes after low-dose alloxan challenge in the mouse (1996)
    Springer
    Diabetologia 39 (1996), S. 383-390 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; alloxan ; atropine ; cholinergic ; mouse ; insulin secretion ; insulin gene expression ; immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The diabetogenic action of the beta-cell toxin, alloxan, is transient when administered to mice at a dosage of 50 mg/kg. We examined whether increased cholinergic activity is involved in the compensatory mechanisms. Therefore, following administration of alloxan, methyl atropine (32 Μmol/kg) was given intraperitoneally once daily for 5 consecutive days. Methyl atropine worsened the degree of hyperglycaemia during the first week after alloxan administration. Recovery from the diabetes mellitus was observed in a substantial number of animals given alloxan without methyl atropine, whereas the risk of developing manifest diabetes was markedly enhanced by methyl atropine. At 35 days after alloxan administration, 33% of the animals, which were given alloxan alone and were diabetic after 4 days, still had diabetes. In contrast, of the animals rendered diabetic by alloxan with concomitant atropinization, 92% remained diabetic throughout the study (p=0.0145 vs alloxan alone). Glucose-stimulated insulin secretion and pancreatic insulin content were markedly reduced in animals with diabetes while being less reduced in alloxan-injected animals without diabetes. Moreover, in situ hybridization and immunocytochemistry revealed markedly decreased levels of insulin mRNA and number of insulin cells in alloxan-treated animals. With regard to insulin secretion, pancreatic insulin content, insulin mRNA and insulin cell number, the reduction was the same irrespective of whether methyl atropine had been given. Thus, 5 days of atropinization increases the incidence of diabetes following alloxan at 50 mg/kg in mice. We suggest that cholinergic activity protects insulin cells from glucotoxicity during the first week after alloxan administration and therefore, reduces the frequency of diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400669
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Blockade of muscarinic transmission increases the frequency of diabetes after low-dose alloxan challenge in the mouse (1996)
    Springer
    Diabetologia 39 (1996), S. 383-390 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetes mellitus ; alloxan ; atropine ; cholinergic ; mouse ; insulin secretion ; insulin gene expression ; immunocytochemistry.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The diabetogenic action of the beta-cell toxin, alloxan, is transient when administered to mice at a dosage of 50 mg/kg. We examined whether increased cholinergic activity is involved in the compensatory mechanisms. Therefore, following administration of alloxan, methyl atropine (32 μmol/kg) was given intraperitoneally once daily for 5 consecutive days. Methyl atropine worsened the degree of hyperglycaemia during the first week after alloxan administration. Recovery from the diabetes mellitus was observed in a substantial number of animals given alloxan without methyl atropine, whereas the risk of developing manifest diabetes was markedly enhanced by methyl atropine. At 35 days after alloxan administration, 33 % of the animals, which were given alloxan alone and were diabetic after 4 days, still had diabetes. In contrast, of the animals rendered diabetic by alloxan with concomitant atropinization, 92 % remained diabetic throughout the study (p = 0.0145 vs alloxan alone). Glucose-stimulated insulin secretion and pancreatic insulin content were markedly reduced in animals with diabetes while being less reduced in alloxan-injected animals without diabetes. Moreover, in situ hybridization and immunocytochemistry revealed markedly decreased levels of insulin mRNA and number of insulin cells in alloxan-treated animals. With regard to insulin secretion, pancreatic insulin content, insulin mRNA and insulin cell number, the reduction was the same irrespective of whether methyl atropine had been given. Thus, 5 days of atropinization increases the incidence of diabetes following alloxan at 50 mg/kg in mice. We suggest that cholinergic activity protects insulin cells from glucotoxicity during the first week after alloxan administration and therefore, reduces the frequency of diabetes. [Diabetologia (1996) 39: 383–390]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400669
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    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Islet amyloid polypeptide in the islets of Langerhans: friend or foe? (2000)
    Springer
    Diabetologia 43 (2000), S. 687-695 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Alloxan-induced diabetes, beta-cell survival, calcitonin receptors, glucose tolerance, IAPP null mutant mice, insulin secretion, receptor-activity-modifying protein (RAMP), transgenic overexpression.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Islet amyloid polypeptide (IAPP), or amylin, was originally discovered as the constituent peptide in amyloid occurring in human insulinomas and in pancreatic islets in human subjects with Type II (non-insulin-dependent) diabetes mellitus. Its normal expression in beta cells and its co-secretion with insulin in response to nutrient stimuli, suggest a metabolic function for the peptide. Specifically, IAPP has most frequently been shown to inhibit insulin secretion, implying that IAPP has a role in the regulation of islet hormone homeostasis. The physiological significance of IAPP in islets has been difficult to assess; very high IAPP concentrations are required to alter insulin secretion. Moreover, until recently, IAPP receptors have not been characterised at the molecular level, thus leaving the actual target cells for IAPP unidentified. Furthermore, in experimental diabetes in rodents, the ratio of IAPP expression to that of insulin invariably is increased. In view of the pleiotropic effects attributed to IAPP, such regulation could be both adverse and beneficial in diabetes. Metabolic characterisation of mice carrying a null mutation in the IAPP gene or which overexpress IAPP in beta cells have recently confirmed that IAPP is a physiological inhibitor of insulin secretion. Based on experiments in which IAPP-deficient mice develop a more severe form of alloxan-induced diabetes, we argue that the action of IAPP in the islets normally is beneficial for beta-cell function and survival; thus, the established up regulation of IAPP expression compared with that of insulin in experimental rodent diabetes could serve to protect islets under metabolically challenging circumstances. [Diabetologia (2000) 43: 687–695]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051364
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Normocalcemia with persistent increase of parathyroid hormone: A prospective study (1992)
    Springer
    Calcified tissue international 51 (1992), S. 27-29 
    Details
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Twelve patients were followed up for 3 months after parathyroidectomy. Serial measurements of serum parathyroid hormone (PTH), calcium, and phosphate were made. Four patients had an increased serum PTH postoperatively, which was already apparent by the third postoperative day. All patients became normocalcemic. Their hyperparathyroid-like phosphate parameters indicated that we were dealing with a biologically active PTH. Using preoperative biochemical parameters it was impossible to predict which patients would have an increased PTH post-parathyroidectomy (PTX). Probably the patients with high PTH post-PTX had higher parathyroid volumes. In our opinion after PTX, a normocalcemic high PTH situation should be avoided by 3 1/2 parathyroid gland extirpation in all cases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296213
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    Paper (German National Licenses)
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  • 10
    Electronic Resource
    Electronic Resource
    Conversion of drug-induced SLE-syndrome by the vasodilating agent cadralazine (1990)
    Springer
    European journal of clinical pharmacology 38 (1990), S. 303-303 
    Details
    ISSN: 1432-1041
    Keywords: cadralazin ; lupus erythematosus ; hydralazine ; SLE-syndrome ; case report ; hypertension ; adverse reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The disappearance of a drug induced SLE syndrome in a 43 year old man, was described. He replaced antihypertensive agent hydralazine by an other vasodilatating agent cadralazine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00315036
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