Daniel M Marko, Meghan O Conn, Jonathan D Schertzer
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引用次数: 0
Abstract
Intermittent fasting (IF) modifies cell- and tissue-specific immunometabolic responses that dictate metabolic flexibility and inflammation during obesity and type 2 diabetes (T2D). Fasting forces periods of metabolic flexibility and necessitates increased use of different substrates. IF can lower metabolic inflammation and improve glucose metabolism without lowering obesity and can influence time-dependent, compartmentalized changes in immunity. Liver, adipose tissue, skeletal muscle, and immune cells communicate to relay metabolic and immune signals during fasting. Here we review the connections between metabolic and immune cells to explain the divergent effects of IF compared with classic caloric restriction (CR) strategies. We also explore how the immunometabolism of metabolic diseases dictates certain IF outcomes, where the gut microbiota triggers changes in immunity and metabolism during fasting.
间歇性禁食(IF)会改变细胞和组织特异性免疫代谢反应,这些反应决定了肥胖和 2 型糖尿病(T2D)期间的代谢灵活性和炎症。禁食迫使新陈代谢变得灵活,并需要增加对不同底物的使用。空腹能在不降低肥胖率的情况下降低代谢炎症和改善葡萄糖代谢,并能影响免疫力随时间发生的分区变化。在禁食期间,肝脏、脂肪组织、骨骼肌和免疫细胞会相互传递代谢和免疫信号。在此,我们回顾了代谢细胞和免疫细胞之间的联系,以解释 IF 与传统热量限制(CR)策略相比的不同效果。我们还探讨了代谢性疾病的免疫代谢是如何决定某些 IF 结果的,其中肠道微生物群在禁食期间引发了免疫和代谢的变化。
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