SLC25A1 may exchange mitochondrial PEP for cytosolic anion

A variety of models assign phosphoenolpyruvate (PEP) generated in the mitochondrial matrix by PCK2 (Phosphoenolpyruvate carboxykinase (GTP), mitochondrial) a role in the regulation of gluconeogenesis and its integration with other aspects of metabolism (e.g., Bluemel et al. 2021; Merrins et al. 2022; Soling et al. 1973; Yu et al. 2021). An attractive recent suggestion is that this process may specifically play a key role in regulating insulin secretion by pancreatic beta cells in response to changing blood glucose levels (Merrins et al. 2022).<br><br>Exchange of citrate for PEP across a membrane has been demonstrated in several model systems (Kleineke et al. 1973; Robinson 1971; Shug & Shrago 1973; Sul et al. 1976; Stipani et al, 1980) but the direction in which it proceeds under physiological conditions and the identity of the protein or proteins that enable this exchange remain unclear, although the citrate transporter SLC25A1 has been identified as a candidate.<br> <br>Here, this hypothetical reaction is annotated as the exchange of mitochondrial PEP for an unspecified cytosolic anion, A-, possibly mediated by SLC25A1.

众多模型将由线粒体基质中由PCK2（磷酸烯醇式丙酮酸羧激酶（GTP），线粒体型）产生的磷酸烯醇式丙酮酸（PEP）在糖异生调节及其与其他代谢方面（例如，Bluemel等，2021；Merrins等，2022；Soling等，1973；Yu等，2021）的整合过程中所扮演的角色进行了分配。近期一个引人注目的观点是，这一过程可能在调节胰岛素分泌方面发挥关键作用，尤其是在胰腺β细胞对血糖水平变化的响应中（Merrins等，2022）。<br><br>在多个模型系统中已证实了通过质膜进行柠檬酸与PEP的交换（Kleineke等，1973；Robinson，1971；Shug & Shrago，1973；Sul等，1976；Stipani等，1980），然而，在生理条件下这一交换过程的方向以及能够实现这种交换的蛋白或蛋白的身份仍不明确，尽管已识别出柠檬酸转运蛋白SLC25A1作为候选者。<br><br>在此，这一假定的反应被标注为线粒体PEP与未指定的细胞质阴离子A-之间的交换，该交换可能由SLC25A1介导。