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  • 1
    Electronic Resource
    Electronic Resource
    Reactive oxygen intermediates in autoimmune islet cell destruction of the NOD mouse induced by peritoneal exudate cells (rich in macrophages) but not T cells (1994)
    Springer
    Diabetologia 37 (1994), S. 22-31 
    Details
    ISSN: 1432-0428
    Keywords: Key words NOD mice, insulitis, reactive oxygen intermediates, superoxide dismutase, peritoneal macrophages.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The non-obese diabetic (NOD) mouse spontaneously develops autoimmune Type 1 (insulin-dependent) diabetes mellitus. NOD mice exhibit massive infiltrates of T cells and macrophages into pancreatic islets (insulitis) prior to diabetes. The contribution of oxygen free radicals to the development of insulitis in NOD mice was examined by administration of its scavengers, such as superoxide dismutase and catalase. Bovine superoxide dismutase and catalase were each coupled to polyethylene glycol. The treatment with superoxide dismutase-polyethylene glycol reduced the number of islets with insulitis and increased the undamaged islet tissue, as compared with the control group. The treatment with catalase-polyethylene glycol showed a similar tendency which did not reach significance. Using a flow cytometric assay of the oxidation of 2′, 7′-dichlorofluorescein, the content of reactive oxygen intermediates in islet cells in the culture system was measured and the effect of peritoneal exudate cells and T cells on their production examined. Peritoneal exudate cells, but not T cells, from NOD mice increased the content of reactive oxygen intermediates in islet cells of either the NOD mouse or the ILI mouse (MHC-identical to NOD); the addition of superoxide dismutase to the culture medium suppressed this increase in NOD or ILI islet cells. The present data support the concept that production of oxygen free radicals mediated by macrophages can damage islet beta cells, directly resulting in autoimmune Type 1 diabetes in NOD mice. [Diabetologia (1994) 37: 22–31]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050067
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Pancreatic Reg/pancreatic stone protein (PSP) gene expression does not correlate with beta-cell growth and regeneration in rats (1994)
    Springer
    Diabetologia 37 (1994), S. 994-999 
    Details
    ISSN: 1432-0428
    Keywords: Pancreas ; growth factors ; gene expression ; beta cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The Reg/pancreatic stone protein (PSP) gene is postulated to be an important regulator of pancreatic beta-cell growth. To investigate this hypothesis, we analysed the expression of the Reg/PSP gene following a 90% pancreatectomy and after chronic glucose infusion, two well-defined models of pancreatic beta-cell growth. There was a rapid induction of the Reg/PSP gene in the remnant pancreas after a 90% pancreatectomy in rats during the period of marked growth of the exocrine and islet tissue. However, a similar rapid, but smaller, induction of the Reg/PSP gene was observed in sham-operated rats and in non-surgical control rats in which there was no enhanced pancreatic growth. Furthermore, there was no pancreatic Reg/PSP gene induction in a model of selective beta-cell growth, the chronic glucose-infused rat. Thus, it is unlikely that Reg/PSP is a beta-cell specific growth factor, even though the function of this important pancreatic gene is still unknown.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400462
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Pancreatic Reg/pancreatic stone protein (PSP) gene expression does not correlate with beta-cell growth and regeneration in rats (1994)
    Springer
    Diabetologia 37 (1994), S. 994-999 
    Details
    ISSN: 1432-0428
    Keywords: Key words Pancreas ; growth factors ; gene expression ; beta cells.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The Reg/pancreatic stone protein (PSP) gene is postulated to be an important regulator of pancreatic beta-cell growth. To investigate this hypothesis, we analysed the expression of the Reg/PSP gene following a 90 % pancreatectomy and after chronic glucose infusion, two well-defined models of pancreatic beta-cell growth. There was a rapid induction of the Reg/PSP gene in the remnant pancreas after a 90 % pancreatectomy in rats during the period of marked growth of the exocrine and islet tissue. However, a similar rapid, but smaller, induction of the Reg/PSP gene was observed in sham-operated rats and in non-surgical control rats in which there was no enhanced pancreatic growth. Furthermore, there was no pancreatic Reg/PSP gene induction in a model of selective beta-cell growth, the chronic glucose-infused rat. Thus, it is unlikely that Reg/PSP is a beta-cell specific growth factor, even though the function of this important pancreatic gene is still unknown. [Diabetologia (1994) 37: 994–999]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400462
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Reactive oxygen intermediates in autoimmune islet cell destruction of the NOD mouse induced by peritoneal exudate cells (rich in macrophages) but not T cells (1994)
    Springer
    Diabetologia 37 (1994), S. 22-31 
    Details
    ISSN: 1432-0428
    Keywords: NOD mice ; insulitis ; reactive oxygen intermediates ; superoxide dismutase ; peritoneal macrophages
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The non-obese diabetic (NOD) mouse spontaneously develops autoimmune Type 1 (insulin-dependent) diabetes mellitus. NOD mice exhibit massive infiltrates of T cells and macrophages into pancreatic islets (insulitis) prior to diabetes. The contribution of oxygen free radicals to the development of insulitis in NOD mice was examined by administration of its scavengers, such as superoxide dismutase and catalase. Bovine superoxide dismutase and catalase were each coupled to polyethylene glycol. The treatment with superoxide dismutase-polyethylene glycol reduced the number of islets with insulitis and increased the undamaged islet tissue, as compared with the control group. The treatment with catalase-polyethylene glycol showed a similar tendency which did not reach significance. Using a flow cytometric assay of the oxidation of 2′, 7′-dichlorofluorescein, the content of reactive oxygen intermediates in islet cells in the culture system was measured and the effect of peritoneal exudate cells and T cells on their production examined. Peritoneal exudate cells, but not T cells, from NOD mice increased the content of reactive oxygen intermediates in islet cells of either the NOD mouse or the ILI mouse (MHC-identical to NOD); the addition of superoxide dismutase to the culture medium suppressed this increase in NOD or ILI islet cells. The present data support the concept that production of oxygen free radicals mediated by macrophages can damage islet beta cells, directly resulting in autoimmune Type 1 diabetes in NOD mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00428773
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Beta-cell ontogeny: growth and death (1997)
    Springer
    Diabetologia 40 (1997), S. B27 
    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/s001250051394
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of diabetes and hypoxia on gene markers of angiogenesis (HGF, cMET, uPA and uPAR, TGF-α, TGF-β, bFGF and Vimentin) in cultured and transplanted rat islets (2000)
    Springer
    Diabetologia 43 (2000), S. 763-772 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetes, islet transplantation, angiogenesis, hepatocyte growth factor and c-MET receptor and urokinase plasminogen activator, bFGF, TGF-β, TGF-α.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. The vascularisation of newly transplanted islets originates from the recipients. Because islets transplanted into a diabetic do less well than those transplanted into a euglycaemic environment, we examined the hypothesis that gene expression of angiogenic factors in grafts is delayed in diabetes. These factors include hepatocyte growth factor (HGF) and its receptor c-MET, and urokinase plasminogen activator (uPA) and its receptor uPAR, basic fibroblast growth factor (bFGF), TGF-α and TGFβ-1.¶Methods. Isolated rat islets were studied in vitro under normoxic and hypoxic culture conditions and gene expression was determined with semi-quantitative multiplex RT-PCR. We found that HGF but not c-MET expression was induced by hypoxia in vitro. Using syngeneic Lewis rats, gene expression was also studied in grafts on days 1, 3, 5, 7 and 14 after transplantation.¶Results. In grafts of normoglycaemic rats, HGF expression was enhanced on day 3 and maintained whereas expression of c-MET fell and remained down until day 14. Expression of uPA was up at day 3 and remained high; expression of uPAR was also up at day 3 but then fell to control levels at day 14. Expression of bFGF, TGF-α and TGFβ-1 persisted throughout. Vimentin, a marker of fibroblasts, had increased expression at day 1 which was further enhanced in subsequent days. In the grafts of diabetic recipients the expression of HGF, uPA and uPAR were delayed, being clearly expressed at day 5 rather than day 3. Vimentin expression was similarly delayed.¶Conclusion/interpretation. This apparent delay in angiogenesis provides a potential mechanism for the less favourable outcomes of islets transplanted into diabetic recipients. [Diabetologia (2000) 43: 763–772]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051374
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  • 7
    Electronic Resource
    Electronic Resource
    Gastrin promotes islet cell growth through interactions with transforming growth factor alpha
    Amsterdam : Elsevier
    Regulatory Peptides 40 (1992), S. 275 
    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(92)90467-9
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  • 8
    Electronic Resource
    Electronic Resource
    The organization of the endocrine pancreas: A hypothetical unifying view of the phylogenetic differences
    Amsterdam : Elsevier
    General and Comparative Endocrinology 38 (1979), S. 28-37 
    Details
    ISSN: 0016-6480
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0016-6480(79)90084-4
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Transcription factor abnormalities as a cause of beta cell dysfunction in diabetes: a hypothesis (1997)
    Springer
    Acta diabetologica 34 (1997), S. 177-184 
    Details
    ISSN: 1432-5233
    Keywords: Key words Diabetes ; Beta cell ; Insulin secretion ; Glucotoxicity ; PDX-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Well-characterized defects in insulin secretion, most notably a loss of glucose-induced insulin secretion, are found in virtually all forms of NIDDM, as well as in early IDDM. Similar abnormalities have been found in all animal models of diabetes in which they have been studied. A novel hypothesis is being proposed to explain the mechanisms responsible for these alterations. Many abnormalities in the various steps of glucose-induced insulin secretion have been identified in rodent models of diabetes, but none by itself seems sufficient to explain the defects. These include a loss of GLUT2, glycogen accumulation, glucose recycling, abnormal glucokinase or hexokinase, altered mitochondrial glycerol phosphate dehydrogenase (mGPDH) activity, abnormal ion channel function and beta cell degranulation. We propose that optimal secretory function is dependent upon the unique differentiation of beta cells that is maintained by a set of transcription factors and that this control is disrupted by the diabetic state. Therefore, we propose that key transcription factors are affected even when beta cells are stressed by insulin resistance in very earliest stages of diabetes and that the abnormality becomes more severe as full-blown diabetes develops, which leads to loss of beta cell differentiation and a resultant derangement of insulin secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005920050071
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  • 10
    Electronic Resource
    Electronic Resource
    A dual population of islets of Langerhans in bovine pancreas (1980)
    Springer
    Cell & tissue research 206 (1980), S. 157-170 
    Details
    ISSN: 1432-0878
    Keywords: Islets of Langerhans ; Islet ontogeny ; Ruminant metabolism ; Cell-to-cell junctions ; B cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary A morphological study of the bovine pancreas from fetus to adult documents the presence of two distinct types of pancreatic islets: large islets, 100 to 1600 μm in diameter, enmeshed in interlobular connective tissue; small islets, 25–200 μm in diameter, enmeshed in exocrine tissue. Large islets consisting primarily of well granulated B cells, decrease in relative volume with increasing age and in the adult are seldom seen. The overall relative volume of endocrine tissue is age dependent and ranges from 30% in the sixth month fetus to 10% in the neonate and 5% in the adult. Small islets contain B cells that increase their cytoplasmic secretory granularity with increasing fetal age, significantly degranulate just prior to birth and subsequently regranulate several weeks after birth. Beta cells of the small islets are uniquely characterized by junctional complexes in close association with large numbers of maculae adherentes (desmosomes). Using lanthanum-hydroxide and freeze-fracture techniques the junctional complexes are shown to consist of macula occludens (focal tight junctions) enclosing nexuses (gap junctions). The two types of islet differ in distribution, times of growth and times of B-cell granularity and may be indicative of functional differences yet to be elucidated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233616
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