Time-limited diets and the gut microbiota in cardiometabolic disease

Abstract

In recent years, intermittent fasting (IF), including periodic fasting and time-restricted feeding (TRF), has been increasingly suggested to constitute a promising treatment for cardiometabolic diseases (CMD). A deliberate daily pause in food consumption influences the gut microbiome and the host circadian clock, resulting in improved cardiometabolic health. Understanding the molecular mechanisms by which circadian host-microbiome interactions affect host metabolism and immunity may add a potentially important dimension to effective implementation of IF diets. In this review, we discuss emerging evidence potentially linking compositional and functional alterations of the gut microbiome with IF impacts on mammalian metabolism and risk of development of hypertension, type 2 diabetes (T2D), obesity, and their long-term micro- and macrovascular complications. We highlight the challenges and unknowns in causally linking diurnal bacterial signals with dietary cues and downstream metabolic consequences and means of harnessing these signals toward future microbiome integration into precision medicine.

Keywords: cardiometabolic disease; circadian rhythms; gut microbiome; intermittent fasting; time-restricted feeding; 心脏代谢性疾病; 昼夜节律; 肠道菌群; 间歇性禁食; 限时进食.

FIGURE 1

Intermittent fasting mediated changes in the gut microbiome composition and function, which in turn may affect cardiometabolic health. Gut microbiome driven WAT browning and lipid absorption contribute to weight management. Microbiome effects on glycemic control through GLP‐1 secretion and β‐cell regeneration. Microbiome derived secondary bile acids activates TGR‐5 to control blood pressure. GLP‐1, glucagon‐like peptide‐1; HDAC3, histone deacetylase 3; Nfil3, nuclear factor interleukin‐3; Ngn3, Neurogenin‐3; SCFA, short chain fatty acids; TGR‐5, Takeda G protein‐coupled receptor 5; WAT, white adipocyte tissue. Figure created with BioRender (biorender.com)

FIGURE 2

Intermittent fasting mediated gut microbial metabolites may affect cardiometabolic complications. IPA, Indole‐3‐propionic acid; SCFA, short chain fatty acids; TGR‐5, Takeda G protein‐coupled receptor 5; TMAO, trimethylamine N‐oxide; TUDCA, tauroursodeoxycholic acid. Figure created with BioRender (biorender.com)