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  • 1
    Electronic Resource
    Electronic Resource
    Histopathological changes in the placenta of streptozotocin induced diabetic rats (1974)
    Springer
    Diabetologia 10 (1974), S. 89-91 
    Details
    ISSN: 1432-0428
    Keywords: Experimental diabetes ; Streptozotocin ; placenta
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Induction of diabetes by one intraperitoneal dose of Streptozotocin (50 mg/kg), 8 to 12 days before mating, was found to produce severe degenerative cystic lesions in the spongiosa layer of the placenta. The administration of Streptozotocin, 16–24 days prior to mating, showed non significant changes in the placenta. The morphologic changes observed might well explain the correlation between the bigger placentas and the smaller fetuses found in the Streptozotocin treated rats. STR administered before mating had no teratogenic effect on the fetuses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00421419
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  • 2
    Electronic Resource
    Electronic Resource
    Severe hyperprolactinaemia is associated with decreased insulin binding in vitro and insulin resistance in vivo (1985)
    Springer
    Diabetologia 28 (1985), S. 138-142 
    Details
    ISSN: 1432-0428
    Keywords: Hyperprolactinaemia ; insulin receptor binding ; monocytes ; erythrocytes ; insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied insulin receptor binding and carbohydrate metabolism in 10 patients with severe hyperprolactinaemia and compared the findings with those obtained in 20 healthy control subjects. Insulin binding to monocytes and erythrocytes was significantly decreased in the patients with an excess of prolactin. Scatchard analysis of binding data indicated that a decrease in the number of receptors rather than in receptor affinity seems to be the prevailing cause of lowered binding in hyperprolactinaemic patients. Furthermore, patients with severe hyperprolactinaemia demonstrated significantly elevated blood glucose levels following oral or intravenous glucose load despite having significantly increased insulin levels after glucose administration. The infusion of insulin induced a delayed hypoglycaemic effect and a decreased inhibition of endogenous insulin secretion, as indicated by the suppression of C-peptide in the hyperprolactinaemic patients. The present data indicate that severe hyperprolactinaemia is associated with an insulin-resistant state, which seems to be caused, at least in part, by a down-regulation of insulin receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00273860
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  • 3
    Electronic Resource
    Electronic Resource
    Thrombogenic factors are related to urinary albumin excretion rate in Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients (1993)
    Springer
    Diabetologia 36 (1993), S. 1045-1050 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; coagulation factors ; lipid peroxides ; endothelial cell ; cardiovascular risk ; diabetic nephropathy ; urinary albumin excretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Parameters of haemostasis, endothelial cell markers and lipid peroxide levels were studied in 64 Type 1 (insulin-dependent) and 94 Type 2 (non-insulin-dependent) diabetic patients according to their urinary albumin excretion rate in comparison with age-matched control subjects. We determined plasma levels of fibrinogen (Clauss' method), coagulation factor VII:activity (clotting assay), factor VII antigen, protein C and S antigen, von Willebrand factor antigen,d-dimer concentration (ELISA), and lipid peroxide levels (thiobarbituric acid) in relation to urinary albumin excretion rate (RIA). Significant positive correlations were found between urinary albumin excretion rate and plasma fibrinogen (p〈0.005,p〈0.02), factor VII activity (p〈0.0002,p〈0.002), factor VII antigen (p〈0.0001,p〈0.001), protein C (p〈0.003,p〈0.05), and lipid peroxides (p〈0.02,p〈0.004) in Type 1 as well as in Type 2 diabetes. Von Willebrand factor (p〈0.001) and protein S (p〈0.0005) correlated with albuminuria only in patients with Type 1 diabetes. Although most of the haemostatic abnormalities are already found in normoalbuminuric patients, the significant positive correlations to urinary albumin excretion indicate that endothelial cell damage and coagulation disorders deteriorate with the progression of diabetic nephropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02374497
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  • 4
    Electronic Resource
    Electronic Resource
    Basal and stimulated plasma levels of pancreatic amylin indicate its co-secretion with insulin in humans (1991)
    Springer
    Diabetologia 34 (1991), S. 52-54 
    Details
    ISSN: 1432-0428
    Keywords: Amylin ; diabetes associated polypeptide ; islet amyloid polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Amylin is a 37-amino acid pancreatic polypeptide, probably involved in the pathophysiology of Type 2 (non-insulin-dependent) diabetes mellitus. We have determined amylin in human plasma by extraction-based radioimmunoassay (Sep-Pak C18). Of 23 healthy control subjects plasma amylin was determined as 11.9+-3.5 ng/l. Of 27 patients with Type 2 diabetes receiving insulin the amylin levels were lower, and in 16 patients with Type 2 diabetes on oral medication they were higher than in the control subjects: 8.2+-4.4 ng/l (p〈0.01) vs 18.8+-9.9 ng/l (p〈0.05). In 14 Type 1 (insulin-dependent) diabetic patients we found extremely low mean amounts of amylin: 2.9+-1.9 ng/l (p〈0.002). Thus, basal amylin appears to be associated with the capacity to release insulin. An oral glucose load stimulated the release of amylin, this was more pronounced in patients with Type 2 diabetes than in healthy subjects. An excellent correlation of mean amylin with mean insulin concentrations was obtained (r=0.949). In patients with Type 2 diabetes amylin was reduced congruent to a decrease in C-peptide during a hyperinsulinaemic, euglycaemic glucose clamp experiment (r=0.971 for linear correlation between C-peptide levels and amylin). We conclude, that amylin and insulin are co-secreted in humans, and that the amylin release is under feedback-control by insulin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404025
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of dexamethasone on insulin sensitivity, islet amyloid polypeptide and insulin secretion in humans (1993)
    Springer
    Diabetologia 36 (1993), S. 84-87 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide ; insulin ; dexamethasone ; insulin resistance ; Type 2 (non-insulin-dependent) diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The response of islet amyloid polypeptide and insulin and their molar ratios were investigated in eight healthy volunteers before and after treatment with dexamethasone by oral and frequently-sampled intravenous glucose tolerance tests. Following dexamethasone treatment the insulin sensitivity index decreased significantly from 6.5±1.3 to 4.1±1.0 (μU·ml−1·min−1, p〈0.05. The area under the curve representing above-basal levels of insulin during oral glucose tolerance test increased significantly following dexamethasone treatment from 48132±9736 to 82230±14846 pmol·l−1·3 h−1, p〈0.05, the area under the curve of islet amyloid polypeptide increased from 1308±183 to 2448±501 pmol·l−1·3h−1, p〈0.05. The overall insulin/islet amyloid polypeptide molar ratios calculated from the area under the curve during the 3-h period of the oral glucose tolerance test was not significantly different before and after dexamethasone treatment (42±5 vs 40±4). During the oral glucose tolerance test the insulin/islet amyloid polypeptide ratio increased significantly from baseline to 30 min (p〈0.05), then declined towards initial values before and after dexamethasone treatment. In conclusion, dexamethasone induced a significant decrease in insulin sensivity and a significant increase in insulin secretion during the oral glucose tolerance test. However, in contrast to previous animal experiments we did not find a change in the insulin/islet amyloid polypeptide ratio before and after dexamethasone treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399099
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  • 6
    Electronic Resource
    Electronic Resource
    Role of islet amyloid polypeptide secretion in insulin-resistant humans (1994)
    Springer
    Diabetologia 37 (1994), S. 188-194 
    Details
    ISSN: 1432-0428
    Keywords: Key words Islet amyloid polypeptide release, insulin secretion, insulin resistance, essential hypertension, obesity.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Although it is generally accepted that islet amyloid polypeptide is cosecreted with insulin, relatively few data on its kinetics are available. We therefore studied the dynamics of islet amyloid polypeptide release following oral and frequently sampled intravenous glucose tolerance tests in comparison to insulin and C-peptide using mathematical model techniques in 14 control subjects, 10 obese and 11 hypertensive patients. The fractional clearance rate of islet amyloid polypeptide (0.034±0.004 min–1 in control subjects, 0.058±0.008 in the obese and 0.050±0.008 in the hypertensive patients) was significantly different (p〈0.01) in each group compared with that of insulin (0.14±0.03 min–1) and similar to that of C-peptide (0.061±0.007 min–1), at least in the insulin-resistant subjects. Based on the insulin sensitivity index derived from the minimal model analysis of intravenous glucose tolerance test data, both the hypertensive (2.4±0.4 min–1/(µU/ml); p〈0.0005) and the obese (2.7±0.5; p〈0.001) patients demonstrated severe insulin resistance compared to control subjects (8.1±1.3). Marked insulin hypersecretion was found in the hypertensive (57.6±5.2 nmol·l–1 in 180 min; p〈0.001) and obese (60.8±10.1; p〈0.003) patients in comparison with control subjects (32.4±3.2). The release of islet amyloid polypeptide was significantly higher in the hypertensive (83.1±16.6 pmol/l in 180 min; p〈0.02) and obese (78.6±13.1; p〈0.005) patients than in control subjects (40.5±6.4). No correlation was found between islet amyloid polypeptide release and the insulin sensitivity index in any group. We conclude that, due to a significantly slower clearance of islet amyloid polypeptide in comparison to insulin, reliance on molar ratios between these two peptides might be misleading in the interpretation of islet amyloid polypeptide secretion especially under non-steady-state conditions. [Diabetologia (1994) 37: 188–194]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050092
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  • 7
    Electronic Resource
    Electronic Resource
    Evaluation of risk factors for the development of nephropathy in patients with IDDM: insertion/deletion angiotensin converting enzyme gene polymorphism, hypertension and metabolic control (1997)
    Springer
    Diabetologia 40 (1997), S. 327-331 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; risk factors ; ACE polymorphism ; glycaemic control ; hypertension.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetic nephropathy represents a major complication in patients with insulin-dependent diabetes mellitus (IDDM). Intervention trials using angiotensin-converting enzyme (ACE) inhibitors have pointed towards the important pathogenetic role of the renin-angiotensin system. Recently an insertion/deletion (I/D) polymorphism for the gene encoding the ACE has been described, the deletion type being associated with higher plasma ACE levels. As the intrarenal renin-angiotensin system might also be activated in this setting, we determined the ACE genotype together with other risk factors for the development of diabetic nephropathy in 122 patients with IDDM from a single centre with (n = 63) and without (n = 59) nephropathy. Long-term glycaemic control was evaluated using mean HbA1c values from the last 10 years. The two patient group were comparable with regard to duration of diabetes and glycaemic control as assessed by current HbA1c values. However, mean long-term HbA1c values were significantly higher in patients with diabetic nephropathy as was systemic blood pressure. The DD genotype was more prevalent in patients with renal disease. In the subgroup of patients who had had diabetes for more than 20 years (n = 90), the DD genotype was even more frequent in patients with nephropathy, and blood pressure and long-term HbA1c values were also higher in patients with renal disease. Logistic regression analysis revealed long-term glycaemic control, blood pressure and the ACE genotype to be independent risk factors for the prevalence of diabetic nephropathy. [Diabetologia (1997) 40: 327–331]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050682
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  • 8
    Electronic Resource
    Electronic Resource
    Decreased insulin receptor binding in hyperthyroidism (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 1074-1080 
    Details
    ISSN: 1432-1440
    Keywords: Hyperthyroidism ; Insulin receptor number ; Carbohydrate metabolism ; Glucose intolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The binding of125I-insulin to insulin receptors on circulating mononuclear leukocytes was studied in ten patients with hyperthyroidism and 20 euthyroid normal volunteers. The hyperthyroid patients demonstrated significantly elevated glucose levels following an oral glucose load, despite normal insulin secretion. The infusion of insulin resulted in a delayed hypoglycaemic effect in the hyperthyroid patients; however, the inhibition of the endogenous insulin secretion as indicated by suppression of C-peptide levels was not different from euthyroid control subjects. Insulin binding to monocytes was significantly decreased in the hyperthyroid patients. Scatchard analysis of binding data indicates that a decrease of receptor number rather than receptor affinity seems to be the cause of the lowered insulin binding in hyperthyroid patients with diffuse toxic goitre. The findings of decreased insulin receptor number, mild degree of glucose intolerance despite normal insulin secretion and the delayed hypoglycaemic effect following insulin infusion suggest that peripheral insulin resistance could be involved in the highly complex pathophysiology of glucose intolerance in hyperthyroidism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01711376
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  • 9
    Electronic Resource
    Electronic Resource
    Besprechungen (1923)
    Springer
    Naturwissenschaften 11 (1923), S. 402-409 
    Details
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01552165
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  • 10
    Electronic Resource
    Electronic Resource
    Primary hyperparathyroidism is associated with decreased insulin receptor binding and glucose intolerance (1984)
    Springer
    Calcified tissue international 36 (1984), S. 253-258 
    Details
    ISSN: 1432-0827
    Keywords: Insulin receptor binding ; Primary hyperparathyroidism ; Hyperinsulinemia ; Monocytes ; Erythrocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We studied insulin receptor-binding and carbohydrate and metabolism in 15 patients with symptomatic primary hyperparathyroidism in comparison with 20 healthy controls. Insulin binding to monocytes and erythrocytes was measured by radioreceptor-ligand-assay. Furthermore, patients and controls were characterized by testing oral (100 g glucose load) glucose tolerance as well as insulin tolerance (0.1U insulin/kg body weight). Compared with controls, patients with primary hyperparathyroidism exhibited marked hyperinsulinemia (P〈0.01) and significantly higher glucose levels (P〈0.01) after an oral glucose load. The glucose lowering effect of intravenous insulin was significantly diminished in primary hyperparathyroidism compared with controls (P〈0.01). Receptor studies revealed a significantly lower (P〈0.01) insulin binding to monocytes and to erythrocytes in patients with primary hyperparathyroidism compared with controls. The present data indicate an insulin-resistant state in primary hyperparathyroidism, which is caused at least in part, by a downregulation of insulin receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405326
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