Abstract
Throughout the day, insulin secretion and biosynthesis result from the activity of numerous β-cells which function in coordination. Until recently, it has been implicitly assumed that all these cells are alike, i.e. that they secrete synchronously and at the same rate under various conditions. However, several lines of evidence now show that the actual situation is more complex. Thus, in situ, individual β-cells show variable amounts of secretory granules and rough endoplasmic reticulum[1], different thresholds for glucose-induced electrical activity[2,3] and a variable ability to biosynthesize insulin[4]. Furthermore, the β-cells located at the periphery of the islets differ from those located in the center of the microorgan with regard to nucleus size[5,6], incorporation of [3H]-thymidine[7], number of gap junctions[8], extent of dye coupling[9], electrical activity[10,11], and ability to secrete insulin[12]. In vitro studies have also revealed marked differences between individual β-cells with respect to insulin release[13–17], electrical activity[18] and Ca2+ changes during stimulation[19,20] as well as with respect to protein biosynthesis[4] and glucose-activated metabolic redox changes[21–23]. This wide heterogeneity, which is reviewed in the first part of this chapter, raises the question of how β-cells achieve the proper coordination which is necessary to ensure appropriate insulin biosynthesis and secretion under continously changing physiological conditions.
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Bosco, D., Meda, P. (1997). Reconstructing Islet Function In Vitro . In: Soria, B. (eds) Physiology and Pathophysiology of the Islets of Langerhans. Advances in Experimental Medicine and Biology, vol 426. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1819-2_39
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DOI: https://doi.org/10.1007/978-1-4899-1819-2_39
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