氨基酸限制改变胰岛β细胞的生存机制：PI3K/Akt 通路的可能作用。
Amino acid restriction alters survival mechanisms in pancreatic beta cells: possible role of the PI3K/Akt pathway.
机构信息
Obesity and Comorbidities Research Center (OCRC), Department of Structural and Functional Biology, Institute of Biology, University of Campinas (UNICAMP), R Carl Von Linnaeus, Campinas, SP, CEP 13083-865, Brazil.
Department of Nutrition and Dietetic, Faculty of Nutrition, Federal Fluminense University, Niteroi, RJ, Brazil.
出版信息
Eur J Nutr. 2021 Oct;60(7):3947-3957. doi: 10.1007/s00394-021-02568-2. Epub 2021 Apr 28.
BACKGROUND AND AIMS
Malnutrition in the early stages of life may lead to changes in the glycemic metabolism during adulthood, such as pancreatic beta cells dysfunction and failure. Therefore, this study aimed to evaluate the effects of an in vitro amino acid restriction model on the function and viability of pancreatic beta cells.
METHODS
Insulin-producing cells (INS-1E) were maintained in control or amino acid restricted culture medium containing 1 × or 0.25 × of amino acids, respectively, for 48 h.
RESULTS
Amino acid restricted group showed lower insulin secretion and insulin gene expression, reduced mitochondrial oxygen consumption rate and reactive oxygen species production. Besides, amino acid restricted group also showed higher levels of endoplasmic reticulum stress and apoptosis markers and enhanced Akt phosphorylation. However, even with higher levels of apoptosis markers, amino acid restricted group did not show higher levels of cell death unless the PI3K/Akt pathway was inhibited.
CONCLUSION
Amino acid restricted beta cell viability seems to be dependent on the PI3K/Akt pathway.
背景与目的
生命早期的营养不良可能导致成年期血糖代谢发生变化，如胰岛β细胞功能障碍和衰竭。因此，本研究旨在评估体外氨基酸限制模型对胰岛β细胞功能和活力的影响。
方法
将胰岛素分泌细胞（INS-1E）分别维持在对照或氨基酸限制培养基中，分别含有 1×或 0.25×的氨基酸，培养 48 小时。
结果
氨基酸限制组胰岛素分泌和胰岛素基因表达降低，线粒体耗氧率和活性氧产生减少。此外，氨基酸限制组内质网应激和细胞凋亡标志物水平升高，Akt 磷酸化增强。然而，即使凋亡标志物水平升高，氨基酸限制组也不会出现更高水平的细胞死亡，除非 PI3K/Akt 通路被抑制。
结论
氨基酸限制的β细胞活力似乎依赖于 PI3K/Akt 通路。
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