Rhodes C J, Taylor K W
Biochem J. 1985 May 15;228(1):87-94. doi: 10.1042/bj2280087.
The direct effects of alpha- and beta-interferons on isolated mouse pancreatic islets were investigated in vitro and found to be similar. After 7 h incubation with interferon concentrations above 350 units/ml, glucose-stimulated (pro)insulin biosynthesis was significantly inhibited, with only a slight inhibition of total protein biosynthesis. Inhibition could be abolished in the additional presence of an anti-interferon antibody. Interferon did not affect insulin release, total insulin content, or glucose oxidation of the islets. The stimulation of (pro)insulin biosynthesis by adenosine, D-glyceraldehyde, mannose, N-acetylglucosamine and leucine was also inhibited by interferon, with no effect on insulin release. At concentrations of dsRNA (double-stranded RNA) said to induce interferon (1-100 micrograms/ml), glucose-stimulated (pro)insulin biosynthesis was inhibited without significantly affecting insulin release. The dsRNA may itself inhibit stimulated (pro)insulin biosynthesis or may function indirectly by the induction of interferon.
在体外研究了α干扰素和β干扰素对分离的小鼠胰岛的直接作用,发现二者作用相似。在与浓度高于350单位/毫升的干扰素孵育7小时后,葡萄糖刺激的(前)胰岛素生物合成受到显著抑制,而总蛋白质生物合成仅受到轻微抑制。在额外存在抗干扰素抗体的情况下,抑制作用可被消除。干扰素不影响胰岛的胰岛素释放、总胰岛素含量或葡萄糖氧化。腺苷、D-甘油醛、甘露糖、N-乙酰葡糖胺和亮氨酸对(前)胰岛素生物合成的刺激也受到干扰素的抑制,而对胰岛素释放无影响。在据说是可诱导干扰素的双链RNA(dsRNA)浓度(1-100微克/毫升)下,葡萄糖刺激的(前)胰岛素生物合成受到抑制,而对胰岛素释放无显著影响。双链RNA本身可能会抑制刺激的(前)胰岛素生物合成,或者可能通过诱导干扰素间接发挥作用。