Iwamoto Tatsuya, Shimizu Shigeomi, Tajima-Sakurai Hajime, Yamaguchi Hirofumi, Nishida Yuya, Arakawa Satoko, Watada Hirotaka
Juntendo Iji Zasshi. 2023 Feb 22;69(1):42-49. doi: 10.14789/jmj.JMJ22-0040-OA. eCollection 2023.
The role of autophagy in pancreatic β cells has been reported, but the relationship between autophagy and insulin metabolism is complex and is not fully understood yet.
We here analyze the relationship between autophagy and insulin metabolism from a morphological aspect.
We observe the morphological changes of β cell-specific Atg7-deficient mice and Atg5-deficient MIN6 cells with electron microscopy.
We find that Atg7-deficient β cells exhibit a marked expansion of the endoplasmic reticulum (ER). We also find that the inhibitory state of insulin secretion causes morphological changes in the Golgi, including ministacking and swelling. The same morphological alterations are observed when insulin secretion is suppressed in Atg5-deficient MIN6 cells.
The defect of autophagy induces ER expansion, and inhibition of insulin secretion induces Golgi swelling, probably via ER stress and Golgi stress, respectively.
自噬在胰腺β细胞中的作用已有报道,但自噬与胰岛素代谢之间的关系复杂,尚未完全明确。
我们从形态学角度分析自噬与胰岛素代谢之间的关系。
我们用电子显微镜观察β细胞特异性Atg7基因敲除小鼠和Atg5基因敲除的MIN6细胞的形态变化。
我们发现Atg7基因敲除的β细胞内质网(ER)明显扩张。我们还发现胰岛素分泌的抑制状态会导致高尔基体形态改变,包括小堆叠和肿胀。当Atg5基因敲除的MIN6细胞中胰岛素分泌受到抑制时,也观察到相同的形态学改变。
自噬缺陷诱导内质网扩张,胰岛素分泌抑制分别通过内质网应激和高尔基体应激诱导高尔基体肿胀。