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  • 1
    Electronic Resource
    Electronic Resource
    Effects of vasoactive intestinal polypeptide (VIP), secretin and gastrin on insulin secretion in the mouse (1981)
    Springer
    Diabetologia 21 (1981), S. 54-59 
    Details
    ISSN: 1432-0428
    Keywords: VIP ; secretin ; gastrin ; basal insulin secretion ; stimulated insulin secretion ; cholinergic stimulation ; β-adrenergic stimulation ; glucose stimulation ; in vivo ; mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The in vivo effects of vasoactive intestinal polypeptide (VIP), secretin and two different molecular forms of gastrin, gastrin 17 and pentagastrin, on basal and stimulated insulin secretion have been investigated in the mouse. All these peptides induced a moderate dose-dependent increase in basal insulin secretion. The different polypeptides showed complex effects on insulin release stimulated by glucose, the cholinergic agonist carbachol or theβ-adrenergic agonist L-isopropylnoradrenaline (L-IPNA), these effects being dependent on the nature of the secretagogue. VIP and secretin both potentiated glucose-induced insulin release. Secretin inhibited insulin secretion induced by carbachol and L-IPNA, whereas VIP potentiated L-IPNA-induced insulin secretion and had no influence on the effect of carbachol. Gastrin 17 and pentagastrin did not affect glucose- or carbachol-induced insulin release, whereas they inhibited L-IPNA-induced insulin secretion. The results suggest that VIP, secretin and gastrin display their effects on insulin secretion through different mechanisms. The results indirectly suggest the existence of separate insulin secretory pathways which operate differently, or at least partly differently, after glucose stimulation, cholinergic stimulation, andβ-adrenergic stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01789115
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  • 2
    Electronic Resource
    Electronic Resource
    Glucagon immunoreactivity in plasma from normal and dystrophic mice (1982)
    Springer
    Diabetologia 22 (1982), S. 258-263 
    Details
    ISSN: 1432-0428
    Keywords: Plasma glucagon ; mice ; muscular dystrophy ; gel filtration ; immunoglobulins ; glucose ; insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present investigation was undertaken to determine and characterize glucagon immunoreactivity in plasma from normal NMRI mice and from dystrophic mice and their unaffected littermates of the 129/ReJ strain. Very young dystrophic mice (6 weeks old) displayed much higher basal levels of plasma glucagon immunoreactivity than normal mice. In contrast, plasma concentrations of insulin and glucose were lower in these dystrophic mice than in normal NMRI mice. The plasma glucagon levels declined with age in both strains during the time-period studied (1.5–5 months). Gel filtration of plasma from dystrophic as well as normal mice on Sephadex G-200 revealed that a large part of the total glucagon immunoreactivity was eluted in fractions containing the immunoglobulins. The amount of the ‘true’ glucagon part was lower in plasma from normal mice (about 0.2 μg/l) than in plasma from mice of the dystrophic strain (0.4–0.5 μg/l)). This finding was indirectly corroborated by the observation that a large intravenous glucose load decreased plasma glucagon by approximately 0.2 μg/l in the non-dystrophic NMRI strain and by about 0.4–0.6 μg/l in the dystrophic strain. Thus, the ability of glucose to suppress glucagon secretion appeared unaffected in the dystrophic mice. Glucose-induced insulin release, however, was considerably impaired in these animals. It is concluded that mice of the dystrophic 129/ReJ strain have higher plasma levels of ‘true’ glucagon than mice of the non-dystrophic NMRI strain. Whether the abnormally high plasma glucagon levels in the dystrophic strain, particularly in very young dystrophic mice, might contribute to the development of the muscular dystrophy remains to be elucidated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00281302
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  • 3
    Electronic Resource
    Electronic Resource
    Erratum (1995)
    Springer
    Diabetologia 38 (1995), S. 47-47 
    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/BF00422380
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  • 4
    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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  • 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. 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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  • 6
    Electronic Resource
    Electronic Resource
    Extensive islet amyloid formation is induced by development of Type II diabetes mellitus and contributes to its progression: pathogenesis of diabetes in a mouse model (1999)
    Springer
    Diabetologia 42 (1999), S. 427-434 
    Details
    ISSN: 1432-0428
    Keywords: Keywords IAPP ; Amylin ; transgenic mice ; ob/ob mice ; insulin resistance ; insulin insufficiency ; islet amyloid ; diabetogenic factor.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Type II (non-insulin-dependent) diabetes mellitus is a multifactorial disease in which pancreatic islet amyloid is a characteristic histopathological finding. Islet amyloid fibrils consist of the beta-cell protein “islet amyloid polypeptide” (IAPP)/“amylin”. Unlike human IAPP (hIAPP), mouse IAPP cannot form amyloid. In previously generated transgenic mice, high expression of hIAPP as such did not induce islet amyloid formation. To further explore the potential diabetogenic role of amyloidogenic IAPP, we introduced a diabetogenic trait (“ob” mutation) in hIAPP transgenic mice. Methods. Plasma concentrations of IAPP, insulin and glucose were determined at 3.5 (t1), 6 (t2), and 16–19 months of age (t3). At t3, the mice were killed and the pancreas was analysed (immuno)histochemically. Results. In non-transgenic ob/ob mice, insulin resistance caused a compensatory increase in insulin production, normalizing the initial hyperglycaemia. In transgenic ob/ob mice, concurrent increase in hIAPP production resulted in extensive islet amyloid formation (more often and more extensive than in transgenic non-ob/ob mice), insulin insufficiency and persistent hyperglycaemia: At t3, plasma insulin levels in transgenic ob/ob mice with amyloid were fourfold lower than in non-transgenic ob/ob mice (p 〈 0.05), and plasma glucose concentrations in transgenic ob/ob mice were almost twofold higher (p 〈 0.05). In addition, the degree of islet amyloid formation in ob/ob mice was positively correlated to the glucose:insulin ratio (r s = 0.53, p 〈 0.05). Conclusion/interpretation. Islet amyloid is a secondary diabetogenic factor which can be both a consequence of insulin resistance and a cause of insulin insufficiency. [Diabetologia (1999) 42: 427–434]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051175
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  • 7
    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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  • 8
    Electronic Resource
    Electronic Resource
    Failure to adequately adapt reduced insulin sensitivity with increased insulin secretion in women with impaired glucose tolerance (1996)
    Springer
    Diabetologia 39 (1996), S. 1099-1107 
    Details
    ISSN: 1432-0428
    Keywords: Insulin secretion ; glucagon secretion ; islet function ; impaired glucose tolerance ; non-insulin-dependent diabetes mellitus ; pathogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To study the islet adaptation to reduced insulin sensitivity in normal and glucose intolerant post-menopausal women, we performed a euglycaemic, hyperinsulinaemic clamp in 108 randomly selected women, aged 58–59 years. Of the 20 women with the lowest insulin sensitivity, 11 had impaired glucose tolerance (IGT) whereas 9 had normal glucose tolerance (NGT). These women together with 15 women with medium insulin sensitivity and 16 women with high insulin sensitivity and NGT were further examined with arginine stimulation at three glucose levels (fasting, 14 and 〉25 mmol/l). In NGT, the acute insulin response (AIR) to 5 g i. v. arginine at all three glucose levels and the slopeAIR, i. e. the glucose potentiation of insulin secretion, were markedly increased in the women with the lowest insulin sensitivity and NGT compared to those with medium or high insulin sensitivity. In contrast, in low insulin sensitivity, AIR was significantly lower in IGT than in NGT (at glucose 14 mmol/l p=0.015, and at 〉25 mmol/l p=0.048). The potentiation of AIR induced by low insulin sensitivity in women with NGT was reduced by 74% (AIR at 14 mmol/l glucose) and 57% (AIR at 〉25 mmol/l glucose), respectively, in women with IGT. Also the slopeAIR was lower in IGT than in NGT (p=0.025); the increase in slopeAIR due to low insulin sensitivity was abolished in IGT. In contrast, glucagon secretion was not different between women with IGT as opposed to NGT. We conclude that as long as there is an adequate beta-cell adaptation to low insulin sensitivity with increased insulin secretory capacity and glucose potentiation of insulin secretion, NGT persists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400660
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  • 9
    Electronic Resource
    Electronic Resource
    Prediction of diabetes using ADA or WHO criteria in post-menopausal women: a 10-year follow-up study (2000)
    Springer
    Diabetologia 43 (2000), S. 1224-1228 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Impaired glucose tolerance, impaired fasting glucose, Type II diabetes, American Diabetes Association, World Health Organisation, progression, oral glucose tolerance test.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To study the risk of women with impaired fasting glucose (IFG) as against impaired glucose tolerance (IGT) developing diabetes.¶Methods. Oral glucose tolerance tests (75 g) were done in 265 women selected at random at baseline (age 55–57 years) and at a 10-year follow-up. Of the women 42 had IFG/NGT (fasting glucose 6.1–6.9 mmol/l, 2-h glucose 〈 7.8 mmol/l), 66 IGT/NFG (2-h glucose 7.8–11.0 mmol/l, fasting glucose 〈 6.1 mmol/l), 30 IGT/IFG and 127 NFG/NGT.¶Results. The 10-year progression to diabetes was similar in IGT/NFG (12.1 %) and IFG/NGT groups (11.9 %, p = 0.97). In IGT/IFG, 20.0 % had developed diabetes, which was not significantly higher than in IFG/NGT and IGT/NFG (p = 0.53). In NFG/NGT at baseline, only 3.9 % had developed diabetes, which was lower than in the other groups (p = 0.023).¶Conclusion/interpretation. Fasting and 2-h glucose concentrations are equally good in predicting diabetes development over a 10-year period in Caucasian postmenopausal women. Because IGT is more common than IFG, measuring only fasting glucose concentrations would, however, result in missing a prediabetic stage in a large group of people at risk for diabetes and cardiovascular diseases. [Diabetologia (2000) 43: 1224–1228]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051516
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  • 10
    Electronic Resource
    Electronic Resource
    Glucose intolerance is predicted by low insulin secretion and high glucagon secretion: outcome of a prospective study in postmenopausal Caucasian women (2000)
    Springer
    Diabetologia 43 (2000), S. 194-202 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Normal glucose tolerance, impaired glucose tolerance, Type II diabetes, insulin sensitivity, insulin secretion, glucagon secretion.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To study the pathophysiological importance of changes in insulin sensitivity and islet function over time for alterations in glucose tolerance in a randomly selected large group of non-diabetic women aged 57–59 years over a 3-year period.¶Methods. At baseline and at the 3-year follow-up, glucose tolerance (WHO 75 g oral glucose), insulin sensitivity (euglycaemic, hyperinsulinaemic clamp) and insulin and glucagon secretion (2 to 5-min responses to 5 g i. v. arginine at fasting, 14 and 〉 25 mmol/l glucose) were measured.¶Results. At baseline, women with impaired glucose tolerance (IGT, n = 28) had lower insulin sensitivity (p = 0.048) than normal women (NGT, n = 58). The arginine-induced insulin responses (AIR) were inversely associated with insulin sensitivity (r≥– 0.55, p 〈 0.001). When related to the 3-year follow-up, the baseline product of AIR at 14 mmol/l glucose times insulin sensitivity, insulin effect index (IE) (r = – 0.40, p 〈 0.001) and the arginine-induced glucagon response at 14 mmol/l glucose (AGR, r = 0.28, p = 0.009) both correlated with follow-up 2-h glucose. In a multiple regression model, baseline 2-h glucose, insulin effect index and arginine-induced glucagon response independently predicted 2-h glucose at follow-up (total r = 0.668, p 〈 0.001). Furthermore, Δinsulin sensitivity (i. e. follow-up minus baseline) correlated with Δinsulin secretion (r = – 0.30, p = 0.006), whereas Δglucagon secretion correlated with Δ2-h glucose (r = 0.30, p = 0.006) over the 3 years. In a multiple regression, alterations in 2-h glucose over the 3 years were independently determined by changes in fasting insulin and glucagon secretion (r = 0.424, p 〈 0.001).¶Conclusion/interpretation. Low insulin secretion, when judged in relation to insulin sensitivity, and high glucagon secretion, determine glucose tolerance over time in the individual subject. These processes are therefore potential targets for prevention of deterioration in glucose tolerance. [Diabetologia (2000) 43: 194–202]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050029
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