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  • 1
    Electronic Resource
    Electronic Resource
    Islet cell antibodies in normal French schoolchildren (1992)
    Springer
    Diabetologia 35 (1992), S. 577-582 
    Details
    ISSN: 1432-0428
    Keywords: Islet-cell antibodies ; prevalence rate ; HLA-DQ region ; Type 1 (insulin-dependent) diabetes mellitus ; children
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet-cell antibodies have been reported to be of predictive value for the future development of Type 1 (insulin-dependent) diabetes in first degree relatives of diabetic patients with the risk increasing in these subjects with the islet-cell antibodies titre. However, very little is known about islet-cell antibodies in background populations. Sera (n= 8363) from schoolchildren (6–17 years) in the French background population were screened for the presence of islet-cell antibodies by the indirect immunofluorescence technique. Islet-cell antibodies greater than 4.5 Juvenile Diabetes Foundation units were found in 150 sera (prevalence rate 1.8%; 95% confidence interval 1.5–2.1%). Only 17 sera demonstrated islet-cell antibody titre 〉-24 JDF units. No particular feature was found to be significantly different between islet-cell antibody-positive and islet-cell antibody-negative children (age, family history of diabetes, fasting plasma glucose, insulin autoantibodies). A second blood sample was obtained from 80 of 150 islet-cell antibody positive children after a mean interval of 8 months. Only 11 sera became 〈 4.5 JDF units with islet-cell antibody titres being stable in the remaining sera, including the high-titre positive sera (〉 24 JDF units). HLA-DQB typing was performed by restriction mapping techniques in 80 islet-cell antibody-positive, in 93 islet-cell antibody-negative and in 213 Type 1 diabetic children. The distribution of the susceptibility alleles (DQB1-Asp57-negative) was not significantly different between islet-cell antibody-positive and islet-cell antibody-negative children. This survey has identified a low islet-cell antibody prevalence rate in French schoolchildren, among whom the incidence rate of Type 1 diabetes is one of the lowest in Europe. The genetic study indicates that part of this group of children are not prone to developing the disease. The predictive value of islet-cell antibodies in normal children will be estimated during the long-term follow-up of this population.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400487
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  • 2
    Electronic Resource
    Electronic Resource
    In utero undernutrition impairs rat beta-cell development (1997)
    Springer
    Diabetologia 40 (1997), S. 1231-1234 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Beta cell ; proliferation ; rat ; nutrition ; immunohistochemistry ; morphometry.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of nutrition on the development of the endocrine pancreas was studied in a rat model obtained by maternal food restriction. A 50 % food restriction was applied to female rats from day 15 of pregnancy and resulted in intrauterine growth-retardation (IUGR) in the offspring. At day 1 postnatal, beta-cell mass was significantly decreased in IUGR pups as compared to controls (0.70 ± 0.06 vs 1.07 ± 0.06 mg, p 〈 0.0001), as well as insulin content. This change in beta-cell mass can be attributed to a reduced number of islets, since the density of insulin-positive aggregates in pancreatic sections of IUGR rats was 20 % lower than in controls. Proliferative capacity of beta cells, as measured by 5-bromo-2-deoxyuridine (BrdU) labelling index, was not altered in growth-retarded animals. Body as well as pancreatic weight were fully recovered in IUGR pups after 21 days of normal feeding by control mothers. However, these animals retained a 25 % decrease in insulin content, 40 % decrease in beta-cell mass (1.58 ± 0.18 vs 2.78 ± 0.42 mg, p 〈 0.001) and a strong reduction in the density of insulin positive aggregates per cm2, as compared to controls, suggesting that the total islet number was likely to be reduced. Beta-cell proliferative capacity remained normal. In conclusion, in utero undernutrition in rats does not impede postnatal growth but durably impairs beta-cell development. Impairment of beta-cell differentiation might be suggested. [Diabetologia (1997) 40: 1231–1234]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050812
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  • 3
    Electronic Resource
    Electronic Resource
    Epidemiology and genetics of diabetic complications (1997)
    Springer
    Diabetologia 40 (1997), S. B62 
    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/s001250051405
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  • 4
    Electronic Resource
    Electronic Resource
    Pathophysiology of diabetic complications (1997)
    Springer
    Diabetologia 40 (1997), S. B65 
    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/s001250051406
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  • 5
    Electronic Resource
    Electronic Resource
    Growth factors and diabetic nephropathy: kidney structure and therapeutic interventions (1997)
    Springer
    Diabetologia 40 (1997), S. B68 
    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/s001250051407
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  • 6
    Electronic Resource
    Electronic Resource
    Enalapril does not alter renal function in normotensive, normoalbuminuric, hyperfiltering Type 1 (insulin-dependent) diabetic children (1989)
    Springer
    Diabetologia 32 (1989), S. 255-260 
    Details
    ISSN: 1432-0428
    Keywords: Angiotensin converting enzyme inhibition ; enalapril ; glomerular hyperfiltration ; diabetic nephropathy ; glomerular filtration rate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Using a prospective randomised double-blind crossover design, the effect of the angiotensin converting enzyme inhibitor enalapril compared to a placebo was studied in 18 normotensive, normoalbuminuric Type 1 (insulin-dependent) diabetic children. Each patient had a high normal or clearly elevated glomerular filtration rate (145 ml· min−1· 1.73 m2 or higher) in the 6 months prior to the study. Enalapril, 0.5 mg·kg−1· day−1, was given for 4 weeks followed by placebo for 4 weeks, or vice versa. At the end of each period, glomerular filtration rate, renal plasma flow, blood pressure, plasma renin activity, and converting enzyme activity were determined. Enalapril caused significant reduction (p=〈0.001) in blood pressure and converting enzyme activity and a rise in plasma renin activity. A slight but not significant rise in glomerular filtration rate and renal plasma flow without change in filtration fraction was observed. These data suggest that the renin angiotensin system is not involved in the glomerular hyperfiltration of Type 1 diabetes, and can be interpreted as showing no evidence for the presence of intraglomerular hypertension in these patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00285294
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  • 7
    Electronic Resource
    Electronic Resource
    A search for tyrosine kinase receptors expressed in the rat embryonic pancreas (1998)
    Springer
    Diabetologia 41 (1998), S. 1474-1481 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Pancreas ; development ; epithelium ; mesenchyme ; receptor tyrosine kinases.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is known that during embryonic life, interactions between the pancreatic epithelium and its surrounding mesenchyme are important for proper development of the pancreas. These interactions are thought to be mediated by soluble factors, which could be, as in other tissues, the ligands of tyrosine kinase receptors. In this study, we screened for tyrosine kinase receptors expressed in pancreata of 13-day-old embryonic rats. Using a polymerase chain reaction-based approach that exploits sequence similarities within the catalytic kinase domains of these receptors, we identified 30 different tyrosine kinase receptors. The same approach was then used on cDNA prepared from fractions enriched in epithelium or in mesenchyme. Receptors for factors such as platelet derived growth factors were found to be expressed both in the epithelial and the mesenchymal fractions. Receptors for stem cell factor, for epidermal growth factor family members were mainly found in the epithelial fraction. The profile of expression of receptor tyrosine kinases in the embryonic pancreas was finally compared to the one found in other tissues and cell types, such as kidney, brain or INS-1 cells. Platelet derived growth factor receptors and ErbB2 were found to be enriched in the embryonic pancreas when compared with other tissues. It will now be possible to test the effects of the ligands of the different receptors we have cloned, on the differentiation and growth of the pancreas. [Diabetologia (1998) 41: 1474–1481]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051094
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  • 8
    Electronic Resource
    Electronic Resource
    Beta-cell mass and proliferation following late fetal and early postnatal malnutrition in the rat (1998)
    Springer
    Diabetologia 41 (1998), S. 1114-1120 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Beta cell ; proliferation ; rat ; nutrition ; immunohistochemistry ; morphometry.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have recently shown that maternal food restriction during late pregnancy in rats decreased beta-cell mass in the offspring at birth, without altering beta-cell proliferation. The aim of the present work was to determine: 1) whether sustained maternal undernutrition until weaning (R group) more dramatically alters beta-cell mass in the offspring and if normal food supply from weaning until adulthood could reverse the deleterious effects and; 2) if altered beta-cell proliferation was responsible for the decreased beta-cell mass. Beta-cell fraction and proliferative capacity were determined during the suckling period and at adult age after ad libitum feeding from weaning in the R animals and in age-matched controls (C group). At day 21, the offspring born and nursed by food-restricted mothers (R animals) showed a 66 % reduction in beta-cell mass and number, which did not increase from birth to weaning, although beta-cell proliferation remained normal. At 3 months of age, R animals had 35 % decreased beta-cell fraction, with a 50 % decrease in the head of the pancreas. In that area, beta-cell proliferation was similar to that of the controls. In the tail of the pancreas, beta-cell fraction was only slightly impaired but beta-cell proliferation was increased by 37 %, as compared with the controls. This increase was associated with a shift in islet size distribution towards medium and large islets compared with the head of pancreas from these R animals. No regional variations of beta-cell fraction, proliferation or islet size distribution were observed in adult control animals. In conclusion, prolonged malnutrition until weaning impairs beta-cell development but not beta-cell proliferation. Subsequent re-nutrition is followed by increased beta-cell proliferation but this is insufficient to fully restore beta-cell mass. [Diabetologia (1998) 41: 1114–1120]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051038
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  • 9
    Electronic Resource
    Electronic Resource
    Effect of ageing on beta-cell mass and function in rats malnourished during the perinatal period (1999)
    Springer
    Diabetologia 42 (1999), S. 711-718 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Malnutrition ; ageing ; beta-cell mass ; apoptosis ; glucose tolerance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. In a recently developed rat model, maternal food restriction from day 15 of pregnancy until weaning induced low birth weight and a 70 % reduction of beta-cell mass in the offspring at day 21 after birth. Subsequent renutrition from weaning was insufficient to fully restore beta-cell mass in young adult rats. The aim of this study is to investigate the long-term consequences of early malnutrition on beta-cell mass and function. Methods. Oral glucose tolerance tests were done in 3- and 12-month-old animals and beta-cell mass and apoptosis were determined by morphometrical measurements on pancreatic sections. The specific impact of postnatal malnutrition was studied by comparing control animals (C group) with animals malnourished during their fetal life only (R/C group), and animals malnourished during fetal life and until weaning (R group). Results. In 3-month-old R/C animals beta-cell mass reached 8.0 ± 1.5 mg with no further increase until 12 months (8.1 ± 1.5 mg), compared with 9.3 ± 1.9 mg in control rats. Twelve-month-old R/C animals showed normal plasma insulin responses and borderline glucose tolerance. In R animals, apoptosis reached 1.9 ± 0.4 % of the beta cells at 3 months, compared with 0.7 ± 0.5 % in control rats, and beta-cell mass did not increase between 3 and 12 months (4.7 ± 0.8 mg at 12 months). In aged control and R animals, apoptosis affected 8 % of the beta cells. At 12 months only, R animals showed profound insulinopenia and marked glucose intolerance. Conclusion/interpretation. In conclusion, perinatal malnutrition profoundly impairs the programming of beta-cell development. In animals with decreased beta-cell mass the additional demand placed by ageing on the beta cells entails glucose intolerance since beta-cell mass does not expand and apoptosis is increased. [Diabetologia (1999) 42: 711–718]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051219
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  • 10
    Electronic Resource
    Electronic Resource
    Insulin-like growth factor-II gene expression in a rat insulin-producing beta-cell line (INS-1) is regulated by glucose (1995)
    Springer
    Diabetologia 38 (1995), S. 927-935 
    Details
    ISSN: 1432-0428
    Keywords: Key words Beta cells ; insulin-like growth factor II ; insulin ; glucose ; gene expression.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A highly differentiated rat glucose-responsive insulin producing cell line INS-1 expresses high levels of insulin-like growth factor-II (IGF-II). Basal levels of IGF-II gene mRNA were expressed in cells cultured at 1–6 mmol/l glucose. At glucose concentrations of 10–20 mmol/l, IGF-II mRNA was increased more than threefold after 44 h of incubation. Levels of IGF-II mRNA in INS-1 cells incubated at 5.6 and 20 mmol/l glucose in the presence of 4 mg/ml actinomycin D are comparable and are not reduced during 20 h of treatment, indicating the high stability of IGF-II mRNA in this cell line. From the three rat IGF-II promoters, promoter 3 is by far the most active in INS-1 cells. The IGF-II promoter 3 activity and IGF-II mRNA production at high glucose concentrations increased threefold over their respective levels at low glucose concentration, suggesting that the glucose-induced IGF-II gene expression in this beta-cell line might be transcriptionally controlled. The up-regulation of IGF-II mRNA by glucose was not due to the increased intracellular cyclic AMP levels or protein kinase C activation. A protein kinase C activator had no effect on IGF-II gene expression, and an adenylate cyclase activator (forskolin), suppressed the stimulatory effects of glucose on the IGF-II mRNA. Under all the experimental conditions examined, the IGF-II and insulin genes were differentially regulated in INS-1 cells. The IGF-II gene expression and DNA synthesis, however, were regulated in parallel, suggesting that these two cellular activities are closely associated. [Diabetologia (1995) 38: 927–935]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400581
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