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  • 1
    Electronic Resource
    Electronic Resource
    Stimulation by glucose of the blood flow to the pancreatic islets of the rat (1983)
    Springer
    Diabetologia 25 (1983), S. 45-50 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic islets ; microcirculation ; glucose-stimulation ; islet blood flow ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Blood flow to the pancreatic islets of the rat was estimated with the microsphere technique. Experiments with microspheres of different sizes (diameter 10, 15 or 50 μm) showed that optimal results were obtained with 10-μm spheres. Localization of microspheres either within or outside the islets was accomplished by freeze-thawing of the pancreas, making it transparent, so that both islets and microspheres could be distinguished in dark field illumination. Thus, microscopic examination of the freeze-thawed pancreas allowed the microspheres to be counted separately in both the endocrine and exocrine parenchyma. Under basal conditions, pancreatic blood flow was calculated as O.60 ml·min-1·g-1 (w/w). The islets accounted for about 10% of the total pancreatic blood flow, corresponding to 0.069 ml/min per whole pancreas. A bolus dose of glucose increased pancreatic blood flow to0.75 ml·min-1·g-1(p 〈0.05), while the fractional islet blood flow rose to 15.1% (p 〈0.001) corresponding to 0.125ml· min-1·pancreas-1 (p·〈0.001). The glucose-induced increase in pancreatic blood flow mainly resulted from increased flow to the pancreatic tail, while the corresponding increase in islet blood flow was uniformly distributed throughout the pancreas. Injection of the non-metabolizable glucose-derivate, 3-0-methyl-D-glucose, affected neither the pancreatic nor the islet blood flow. The data indicate that the islets receive more of the pancreatic blood flow than would be accounted for by their relative volume and that glucose preferentially stimulates blood flow to the islets.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00251896
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The life story of the pancreatic B cell (1984)
    Springer
    Diabetologia 26 (1984), S. 393-400 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic B cell ; pancreatic islet ; B-cell differentiation ; islet blood flow ; B-cell proliferation ; B-cell cycle ; hereditary diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Most research on the pancreatic B cell has so far focussed on the regulation and molecular biology of insulin biosynthesis and release. The present review draws attention to some additional areas of islet research which have become accessible to investigation by recent methodological progress and which may advance our understanding of the role of the B cell in diabetes. There is now evidence to suggest that B cells arise from a pool of undifferentiated precursor cells in the fetal and newborn pancreas. These cells may contribute to islet growth and, if inappropriately stimulated, also to early islet hyperplasia. In the postnatal state, B-cell function is finely tuned by a complex set of incoming signals, one of which is the nutrient supply provided by the blood. Recent studies indicate that a disproportionately high fraction of pancreatic blood is diverted to the islets and that the islet blood flow is increased by glucose. An acute stimulus to insulin release may thus be accompanied by a process which enhances the distribution of the hormone to the target cells. Long-term adjustments of B-cell function are made by changes in B-cell number and total mass. Adaptive growth responses to an increased insulin demand occur in a number of hereditary diabetic syndromes in animals, but in some of these there is an inherited restriction on the capacity for B-cell proliferation leading to further deterioration of the glucose tolerance. Some evidence suggests that a similar mechanism may operate also in human non-insulin-dependent diabetes. A critical appraisal of this hypothesis requires, however, that human B cells should be tested for their growth characteristics. Studies of B-cell proliferation in experimental animals have shown that the B cell passes through the cell cycle at a relatively high rate but that the fraction of proliferating cells is low. Regulation of growth of the total B-cell mass seems to take place by changes in the number of B cells passing through the cell cycle rather than by changes in the rate of the cycle. The number of proliferating B cells also shows a marked decrease with age. It is at present uncertain to what extent these regulatory mechanisms apply also to the human B cell but it can be anticipated that further technical developments will elucidate this problem.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00262208
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    Paper (German National Licenses)
    Fulltext
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