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Studies of the postnatal growth of the beta-cell mass in rats have revealed some unexpected and apparently paradoxical results, the most prominent being a beta-cell mass plateau in the early phase of life. We have studied the postnatal growth of the beta-cell mass in the domestic pig to investigate its development in a larger mammal. The pancreases from a total of 86 male pigs from 5 to 100 days of age were studied. The beta-cell mass increased linearly from day 5 to day 40, reached a plateau from day 40 to day 60, and then increased further into adulthood. The relative beta-cell mass (beta-cell mass per body mass) was increased in the early postnatal period but reached a constant level from day 60, after which there was a linear relationship between the beta-cell mass and the body mass. There were high rates of both beta-cell apoptosis and mitosis at 50 and 60 days of age, while the Volume-weighted mean islet Volume increased from birth and reached a plateau at approximately 60 days of age. A beta-cell mass plateau early in life accompanied by a wave of beta-cell apoptosis coinciding with the relative beta-cell mass decreasing to reach a constant level, and a linear relationship between the beta-cell mass and the body mass in later life is exactly what has previously been reported in rats. The coincidence of these events in both rats and pigs, although occurring at different ages in the two species, suggests a causal relationship as previously suggested in a proposed explanatory model for postnatal beta-cell growth.
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ABSTRACT
Fusidic acid and its sodium salt (fusidin) are antistaphylococcal drugs with a steroidal primary structure. Both compounds have been shown to prevent the lymphocyte co-stimulatory activities of the cytokines, interleukin (IL)-1 and IL-6, in a manner similar to that of cyclosporin A. As shown in this paper, fusidin also prevents the inhibitory effect of human recombinant IL-1β (rIL-1β) and the stimulatory effect of human rIL-6, on glucose-induced insulin production in vitro by normal rat pancreatic islets. The drug also inhibited rIL-1β-induced IL-6 production by the islets. Fusidin showed a dose-related effect at pharmacologically relevant concentrations from 3 to 30 μg/ml, and the drug was progressively less active when added 1, 4 and 24 h after rIL-1β. Electron microscopical studies showed that β cells cultured for 72 h with rIL-1β accumulated less lipid in the presence of fusidin, most probably reflecting the functionally protective effect of the drug. Other characteristic ultrastructural changes induced in β cells by rIL-1β were, however, not altered. It is suggested that fusidin may prove clinically effective as a modulator of IL-1- and IL-6-induced changes in β-cell functions.
Journal of Endocrinology (1992) 132, 345–352
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Abstract
Studies of individual cell types in the islets of Langerhans are complicated by the cells' functional coupling by gap junctions and paracrine interaction. Access to purified alpha and beta cells is therefore desirable. We present a simplified and optimized method for fluorescence-activated cell sorting of endocrine pancreatic rat islets. For dispersion of the islets, dispase was superior to trypsin, as the number of vital single cells was higher (1·1 ± 0·1 × 103 vs 0·6 ± 0·1 × 103/islet, P<0·05). The purity of the sorted cells was 96·7 ± 1·2% for the non-beta cells and 97·8 ± 0·6% for the beta cells (numbers in percentages of endocrine cells). In culture, isolated beta cells, non-beta cells and mixtures of beta and non-beta cells formed aggregates, but not at low temperature (4 °C) and not in medium with low serum content (2%). Finally, in pure beta cell aggregates, glucose stimulated changes in cytoplasmic free Ca2+ concentration although both glucose- and arginine-induced insulin secretion was much reduced. We conclude that alpha cells are necessary for insulin secretion but not for glucose sensing.
Journal of Endocrinology (1996) 149, 145–154