期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：27
页码：10090-10094
DOI：10.1073/pnas.0403551101
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：In type 1 diabetes (T1D), there is a specific destruction of the insulin secreting pancreatic {beta} cell. Although the exact molecular mechanisms underlying {beta} cell destruction are not known, sera from T1D patients have been shown to promote Ca2+-induced apoptosis. We now demonstrate that apolipoprotein CIII (apoCIII) is increased in serum from T1D patients and that this serum factor both induces increased cytoplasmic free intracellular Ca2+ concentration ([Ca2+]i) and {beta} cell death. The apoCIII-induced increase in [Ca2+]i reflects an activation of the voltage-gated L-type Ca2+ channel. Both the effects of T1D sera and apoCIII on the {beta} cell are abolished in the presence of antibody against apoCIII. Increased serum levels of apoCIII can thus account for the increase in {beta} cell [Ca2+]i and thereby {beta} cell apoptosis associated with T1D.
