期刊名称：Journal of Nutritional Science and Vitaminology
印刷版ISSN：0301-4800
电子版ISSN：1881-7742
出版年度：2020
卷号：66
期号：2
页码：168-175
DOI：10.3177/jnsv.66.168
出版社：Center for Academic Publications Japan
摘要：A maternal low-protein diet increases the susceptibility of offspring to type 2 diabetes by inducing alterations in β cell mass and function. However, the mechanism of this pancreas injury remains poorly understood. The present study aimed to assess whether autophagy is altered in the pancreas of intrauterine growth restriction (IUGR). In addition, the autophagy associated mammalian target of rapamycin complex 1 (mTORC1) signaling and endoplasmic reticulum (ER) stress were further evaluated in the pancreas. The maternal protein restriction IUGR rat model was established as the IUGR group, and assessed alongside normal newborn rats (CON group). Then, the levels of autophagy markers were assessed by transmission electron microscopy, immunofluorescence, quantitative real-time PCR (qRT-PCR) and Western blot, respectively. In addition, mTORC1 signaling effectors were evaluated by Western blot; ER stress was quantitated by immunohistochemistry, qRT-PCR and Western blotting. Compared with the control group, the IUGR group showed increased levels of the autophagy markers LC3II and Beclin1, with decreased mTORC1 signaling activity. In addition, ER stress was confirmed in β cells of the IUGR group. These findings provided evidence that maternal protein restriction enhances autophagy in newborn pancreas, where ER stress was also induced in β cells, which might effect the pancreas development.
