Intermittent fasting influences immunity and metabolism.

Obesity compromises metabolic flexibility and increases specific immune responses. Fasting forces metabolic flexibility and alters glucose, fatty acids, glycerol, and amino acids to maintain blood glucose and energy balance. Intermittent fasting (IF) lowers inflammation and opposes metabolic dysfunction during obesity. IF can improve glucose metabolism independent of changes in obesity. Gut microbiota composition altered by IF triggers changes in immunity and metabolism. 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. [ABSTRACT FROM AUTHOR]