Impaired Ca2+ response to glucose in mouse β-cells infected with Coxsackie B or Echo virus

Uppsala University, Uppsala, Uppsala, Sweden
Virus Research (Impact Factor: 2.32). 10/1994; 33(3):229-40. DOI: 10.1016/0168-1702(94)90105-8
Source: PubMed

ABSTRACT Five strains of Coxsackie B4 virus and one of Echo 11 virus were tested with regard to their ability to replicate in pancreatic mouse beta-cells and interfere with the alterations of the cytoplasmic Ca2+ concentration ([Ca2+]i) induced by glucose. All strains except one both multiplied and caused cytopathic effect. In a control group 68% of the beta-cells responded to 11 mM glucose with large amplitude oscillations of [Ca2+]i. After inoculation with the infectious strains these oscillations appeared in only 5% of the beta-cells, whereas the non-infectious strain did not modify the glucose effect on [Ca2+]i. Despite the virus interference with the glucose response, [Ca2+]i was increased after depolarization with excessive extracellular K+ and the oscillations were induced in most beta-cells when glucose was combined with the insulin-releasing sulfonylurea tolbutamide.

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    • "Infections with the coxsackievirus serotype B4 (CB4) have been etiologically linked to type 1 diabetes in humans , and CB4 was isolated from patients who died shortly after being diagnosed with the disease (Szopa et al., 1993). Several CB4 isolates can infect human and murine pancreatic ␤-cells and cause cellular dysfunction and/or death in vitro (Frisk et al., 1994; Roivainen et al., 2000; Szopa et al., 1986, 1990; Yoon et al., 1979). Moreover , some clinical isolates, after several passages through mouse pancreatic ␤-cell cultures, fulfilled Koch's postulate by inducing a diabetes-like syndrome in susceptible strains of mice (Toniolo et al., 1982; Yoon et al., 1978). "
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