Intermittent fasting influences immunity and metabolism

被引：10
作者：
Marko, Daniel M. [1 ,2 ,3 ]
Conn, Meghan O. [1 ,2 ,3 ]
Schertzer, Jonathan D. [1 ,2 ,3 ]
机构：
[1] McMaster Univ, Dept Biochem & Biomed Sci, Hamilton, ON, Canada
[2] McMaster Univ, Farncombe Family Digest Hlth Res Inst, Hamilton, ON, Canada
[3] McMaster Univ, Ctr Metab Obes & Diabet Res, Hamilton, ON, Canada
来源：
TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2024年 / 35卷 / 09期
基金：
加拿大健康研究院;
关键词：
CALORIC RESTRICTION; ENERGY-EXPENDITURE; WEIGHT-LOSS; OBESITY; HEALTH; GLUCOSE; FLEXIBILITY; HOMEOSTASIS; MICROBIOTA; HUMANS;
D O I：
10.1016/j.tem.2024.04.014
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
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.
引用
收藏
页码：821 / 833
页数：13
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