Šrámek Jan, Němcová-Fürstová Vlasta, Kovář Jan
Division of Cell and Molecular Biology & Center for Research of Diabetes, Metabolism and Nutrition, Third Faculty of Medicine, Charles University in Prague, Ruská 87, Prague 11000, Czech Republic.
Int J Mol Sci. 2016 Sep 12;17(9):1400. doi: 10.3390/ijms17091400.
Pancreatic β-cell failure and death is considered to be one of the main factors responsible for type 2 diabetes. It is caused by, in addition to hyperglycemia, chronic exposure to increased concentrations of fatty acids, mainly saturated fatty acids. Molecular mechanisms of apoptosis induction by saturated fatty acids in β-cells are not completely clear. It has been proposed that kinase signaling could be involved, particularly, c-Jun N-terminal kinase (JNK), protein kinase C (PKC), p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt kinases and their pathways. In this review, we discuss these kinases and their signaling pathways with respect to their possible role in apoptosis induction by saturated fatty acids in pancreatic β-cells.
胰腺β细胞功能衰竭和死亡被认为是2型糖尿病的主要原因之一。除高血糖外,长期暴露于浓度升高的脂肪酸(主要是饱和脂肪酸)也会导致这种情况。饱和脂肪酸诱导β细胞凋亡的分子机制尚不完全清楚。有人提出激酶信号可能参与其中,特别是c-Jun氨基末端激酶(JNK)、蛋白激酶C(PKC)、p38丝裂原活化蛋白激酶(p38 MAPK)、细胞外信号调节激酶(ERK)以及Akt激酶及其信号通路。在这篇综述中,我们讨论了这些激酶及其信号通路在饱和脂肪酸诱导胰腺β细胞凋亡中可能发挥的作用。