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  • 1
    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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  • 2
    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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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Cell cycle and gene expression in the insulin producing pancreatic cell line βTC1 (1990)
    Springer
    Diabetologia 33 (1990), S. 586-592 
    Details
    ISSN: 1432-0428
    Keywords: Beta cell growth ; cell cycle ; oncogenes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The pancreatic cell line βTC1, established from insulinomas of transgenic mice carrying a hybrid insulin-promoted large T antigen gene, has retained several characteristics of normal cells, including the insulin content and inducibility of insulin secreting by glucose. We show here that the growth of βTC1 cells is arrested in low serum-concentration medium. Cells exposed for three days to 0.25% fetal calf serum ceased to incorporate [3H] thymidine but were still able to resume the cell division cycle upon addition of serum. In this cell line, we have determined by cytofluorometry the cell cycle kinetic parameters to be of 21 h, 10 h 30 min and 12 h for the G1, S and G2/M phases, respectively. Quiescent βTC1 cells constitutively expressed the protooncogene c-jun that codes for the transcriptional factor AP1, as well as cdc2, another cell cycle-related gene. A large transient increase in the expression of the c -fos gene was obtained rapidly, 30 min after addition of serum and a similar increase in c-jun expression after one hour. Expression of the cdc2 gene was also enhanced to a lesser extent. The same effects were also observed in the presence of cycloheximide, thus proving that the expression of these three genes is directly stimulated by serum growth factors. Consequently, quiescent βTC1 cells provide a good model for studying the short- and long-term effects of growth factors on Beta-cell proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400201
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  • 5
    Electronic Resource
    Electronic Resource
    Conference paper(s)
    Amsterdam : Elsevier
    Prostaglandins 27 (1984), S. 40 
    Details
    ISSN: 0090-6980
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0090-6980(84)90285-5
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  • 6
    Electronic Resource
    Electronic Resource
    Differentiation of newborn rat preadipocytes in culture: Effects of insulin and dexamethasone
    Amsterdam : Elsevier
    Experimental Cell Research 191 (1990), S. 133-140 
    Details
    ISSN: 0014-4827
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0014-4827(90)90046-D
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  • 7
    Electronic Resource
    Electronic Resource
    Perinatal Malnutrition Programs Sympathoadrenal and Hypothalamic-Pituitary-Adrenal Axis Responsiveness to Restraint Stress in Adult Male Rats (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 14 (2002), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In humans, an altered control of cortisol secretion was reported in adult men born with a low birth weight making the hypothalamic-pituitary-adrenal (HPA) axis a possible primary target of early life programming. In rats, we have recently shown that maternal food restriction during late pregnancy induces both an intrauterine growth retardation and an overexposure of fetuses to maternal corticosterone, which disturb the development of the HPA axis in offspring. The first aim of this work was to investigate, in adult male rats, whether perinatal malnutrition has long-lasting effects on the HPA axis activity during both basal and stressful conditions. Moreover, as the HPA axis and sympathetic nervous system are both activated by stress, the second aim of this work was to investigate, in these rats, the adrenomedullary catecholaminergic system under basal and stressful conditions. This study was conducted on 4-month-old male rats malnourished during their perinatal life and on age-matched control animals. Under basal conditions, perinatal malnutrition reduced body weight and plasma corticosteroid-binding globulin (CBG) level but increased mineralocorticoid receptor (MR) gene expression in CA1 hippocampal area. After 30 min of restraint, perinatally malnourished (PM) rats showed increased plasma noradrenaline, adrenocorticotropin hormone (ACTH) and corticosterone concentrations similarly as controls, but calculated plasma-free corticosterone concentration was significantly higher and adrenaline level lower than controls. During the phase of recovery, PM rats showed a rapid return of plasma ACTH and corticosterone concentrations to baseline levels in comparison with controls. These data suggest that in PM rats, an elevation of basal concentrations of corticosterone, in face of reduced CBG and probably increased hippocampal MR lead to a much larger impact of corticosterone on target cells that mediate the negative-feedback mechanism on the activities of both the HPA axis and sympathoadrenal one.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0007-1331.2001.00753.x
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  • 8
    Electronic Resource
    Electronic Resource
    VIP receptors: covalent labeling and molecular identification
    Amsterdam : Elsevier
    Regulatory Peptides 6 (1983), S. 314 
    Details
    ISSN: 0167-0115
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0167-0115(83)90207-0
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