Direct and indirect evidences show that elevated glucose concentrations in airway surface liquid (ASL) promote lung infection by pathogens, playing a role in the progression of the Cystic Fibrosis (CF) disease. The joint action of transporter/s for glucose and of the cellular enzymes is essential in order to try to lower ASL glucose level. Inside the cell, the glycolysis and the pentose phosphate pathway (PPP) compete for the utilization of glucose-6-phosphate (G6P), the product in which glucose, after entry within the cell and phosphorylation, is trapped. The study aims to clarify whether, modulating the activity of enzymatic proteins and/or the level of metabolites/cofactors, involved in intracellular glucose utilization, a lowering of the extracellular glucose level in CF occurs. Biochemical approaches have enabled us to understand i) how G6P is shunted between glycolysis and PPP and ii) that mitochondria, more than enzymes/cofactors participating to the two cell glucose utilization pathways, are protagonists of the scene in counteracting the high ASL glucose level as well as oxidative stress in CF.

中文翻译：

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葡萄糖相关代谢途径的调节控制气道表面液体中的葡萄糖水平并与囊性纤维化细胞中的氧化应激作斗争。

直接和间接的证据表明，气道表面液（ASL）中葡萄糖浓度的升高促进了病原体的肺部感染，在囊性纤维化（CF）疾病的进展中起作用。为了尝试降低ASL葡萄糖水平，转运蛋白对葡萄糖和细胞酶的联合作用是必不可少的。在细胞内部，糖酵解和磷酸戊糖途径（PPP）竞争利用6-磷酸葡萄糖（G6P）的产物，其中葡萄糖进入细胞并被磷酸化后被困在其中。该研究旨在阐明是否通过调节酶蛋白的活性和/或代谢物/辅因子的水平来参与细胞内葡萄糖的利用，从而降低CF中细胞外葡萄糖的水平。