Glucose Load Following Prolonged Fasting Increases Oxidative Stress-Linked Response in Individuals With Diabetic Complications

内分泌学 内科学 氧化应激 谷胱甘肽还原酶 2型糖尿病 医学 谷胱甘肽过氧化物酶 线粒体生物发生 胰岛素抵抗 糖尿病 柠檬酸合酶 谷胱甘肽 线粒体 生物 生物化学 超氧化物歧化酶
作者
Ekaterina von Rauchhaupt,Claus Rodemer,Elisabeth Kliemank,Ruben Bulkescher,Marta Campos,Stefan Kopf,Stefan Kopf,Stephan Herzig,Peter Nawroth,Julia Szendroedi,Johanna Zemva,Alba Sulaj
出处
期刊:Diabetes Care [American Diabetes Association]
标识
DOI:10.2337/dc24-0209
摘要

OBJECTIVE Prolonged catabolic states in type 2 diabetes (T2D), exacerbated by excess substrate flux and hyperglycemia, can challenge metabolic flexibility and antioxidative capacity. We investigated cellular responses to glucose load after prolonged fasting in T2D. RESEARCH DESIGN AND METHODS Glucose-tolerant individuals (CON, n = 10), T2D individuals with (T2D+, n = 10) and without diabetes complications (T2D−, n = 10) underwent oral glucose tolerance test before and after a 5-day fasting-mimicking diet. Peripheral blood mononuclear cells’ (PBMC) resistance to ex vivo dicarbonyl methylglyoxal (MG) exposure after glucose load was assessed. Markers of dicarbonyl detoxification, oxidative stress, and mitochondrial biogenesis were analyzed by quantitative PCR, with mitochondrial complex protein expression assessed by western blotting. RESULTS T2D+ exhibited decreased PBMC resistance against MG, while T2D− resistance remained unchanged, and CON improved postglucose load and fasting (−19.0% vs.−1.7% vs. 12.6%; all P = 0.017). T2D+ showed increased expression in dicarbonyl detoxification (mRNA glyoxalase-1, all P = 0.039), oxidative stress (mRNA glutathione-disulfide-reductase, all P = 0.006), and mitochondrial complex V protein (all P = 0.004) compared with T2D− and CON postglucose load and fasting. Citrate synthase activity remained unchanged, indicating no change in mitochondrial number. Mitochondrial biogenesis increased in T2D− compared with CON postglucose load and fasting (mRNA HspA9, P = 0.032). T2D−, compared with CON, exhibited increased oxidative stress postfasting, but not postglucose load, with increased mRNA expression in antioxidant defenses (mRNA forkhead box O4, P = 0.036, and glutathione-peroxidase-2, P = 0.034), and compared with T2D+ (glutathione-peroxidase-2, P = 0.04). CONCLUSIONS These findings suggest increased susceptibility to glucose-induced oxidative stress in individuals with diabetes complications after prolonged fasting and might help in diet interventions for diabetes management.
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