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  • Key words Islet amyloid polypeptide release, insulin secretion, insulin resistance, essential hypertension, obesity.  (1)
  • Nifedipine  (1)
  • Type 1 diabetes  (1)
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  • 1
    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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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Long-term treatment with nifedipine reduces urinary albumin excretion and glomerular filtration rate in normotensive type 1 diabetic patients with microalbuminuria (1994)
    Springer
    Acta diabetologica 31 (1994), S. 14-18 
    Details
    ISSN: 1432-5233
    Keywords: Microalbuminuria ; Calcium channel blockers ; Nifedipine ; Type 1 diabetes ; Diabetic nephropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present study was to investigate the renal effects of long-term treatment with the calcium channel blocker nifedipine in normotensive type 1 diabetic patients with microalbuminuria. In a randomized, double-blind trial, 15 type 1 diabetic patients were treated with either nifedipine (n=8; dosage 30 mg/day) or placebo (n=7) for 12 months. At baseline and after 6 and 12 months of therapy, the albumin excretion rate (UAER, radioimmunoassay), glomerular filtration rate (GFR, chromium 51 ethylenediamine tetra-acetic acid clearance) and renal plasma flow (RPF, iodine 125 hippuran clearance) were determined. Nifedipine treatment caused a significant reduction of UAER after 6 and 12 months (median, Q1/Q3 in mg/24 h): baseline 84 (65/163); 6 months 35 (23/90),P〈0.02; 12 months 39 (15/79),P〈0.05. GFR was significantly decreased by nifedipine treatment (baseline 157±15, 6 months 122±8, 12 months 111±47 ml/min;P〈0.05, mean ± SEM), whereas RPF remained constant. Nifedipine treatment did not influence systolic (baseline 121±7, 12 months 124±2 mmHg, mean ± SEM) or diastolic (baseline 72±2, 12 months 74±3 mmHg) arterial blood pressure. With placebo treatment no significant alterations of UAER, GFR, RPF and arterial blood pressure were observed. Metabolic control was constant throughout the whole study period. Thus, 1 year's treatment with nifedipine reduces the UAER and GFR in normotensive type 1 diabetic patients without influencing the systemic arterial blood pressure. The data, however, do not present a recommendation for the general use of nifedipine in these patients as the exact intrarenal mechanism of calcium channel blockers in humans remains to be established.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00580754
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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