胰腺贝塔细胞具备分泌胰岛素并以此降血糖的功能。日本研究人员发现，胰腺贝塔细胞有一种内在机制可以防止其“过劳死”，有可能利用这一机制开发出防治糖尿病的药物。
日本东北大学石原寿光等人在新一期美国《Cell Metabolism》杂志网络版上发表论文说，他们的研究显示，一旦胰腺贝塔细胞工作负担过重，它们内部就会大量合成一种名为“4E－BP1”的蛋白质。这种蛋白质可以防止胰腺贝塔细胞过度劳作。
研究人员让实验鼠不能合成“4E－BP1”蛋白质，结果实验鼠体内的胰腺贝塔细胞在持续超负荷工作的情况下相继死亡，实验鼠产生胰岛素的能力减弱，血糖值出现上升。
研究人员认为，如能在新发现的基础上开发出防止胰腺贝塔细胞过度劳作的药物，这类药物也许可以用来防止糖尿病发病或病情恶化。
原始出处：
Cell Metabolism, Vol 7, 269-276, 05 March 2008
ATF4-Mediated Induction of 4E-BP1 Contributes to Pancreatic β Cell Survival under Endoplasmic Reticulum Stress
Suguru Yamaguchi, Hisamitsu Ishihara, Takahiro Yamada, Akira Tamura, Masahiro Usui, Ryu Tominaga, Yuichiro Munakata, Chihiro Satake, Hideki Katagiri, Fumi Tashiro, Hiroyuki Aburatani, Kyoko Tsukiyama-Kohara, Jun-ichi Miyazaki, Nahum Sonenberg, and Yoshitomo Oka
Summary
Endoplasmic reticulum (ER) stress-mediated apoptosis may play a crucial role in loss of pancreatic β cell mass, contributing to the development of diabetes. Here we show that induction of 4E-BP1, the suppressor of the mRNA 5′ cap-binding protein eukaryotic initiation factor 4E (eIF4E), is involved in β cell survival under ER stress. 4E-BP1 expression was increased in islets under ER stress in several mouse models of diabetes. The Eif4ebp1 gene encoding 4E-BP1 was revealed to be a direct target of the transcription factor ATF4. Deletion of the Eif4ebp1 gene increased susceptibility to ER stress-mediated apoptosis in MIN6 β cells and mouse islets, which was accompanied by deregulated translational control. Furthermore, Eif4ebp1 deletion accelerated β cell loss and exacerbated hyperglycemia in mouse models of diabetes. Thus, 4E-BP1 induction contributes to the maintenance of β cell homeostasis during ER stress and is a potential therapeutic target for diabetes.
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