Published online Jun 14, 2025. doi: 10.3748/wjg.v31.i22.108815
Revised: May 10, 2025
Accepted: May 26, 2025
Published online: June 14, 2025
Processing time: 49 Days and 16.3 Hours
Intermittent fasting (IF), particularly time-restricted feeding (TRF), is increasingly popular has gained popularity for weight loss, yet management, but its effects impact on gut health remain unclear. Remains inadequately understood. This study explores how investigated the effects of TRF effects on intestinal health and explored the underlying mechanisms.
To assess the effects of IF on intestinal health, elucidate the mechanisms involved.
Mice were divided into two groups: Normal control (NC) and IF. The IF group underwent TRF, while the NC group had unrestricted access to food. Body weight, fecal characteristics, and intestinal morphology were analyzed. Colon tissue, serum, and fecal samples were collected for histological analysis, enzyme-linked immunosorbent assay, flow cytometry, 16S rRNA sequencing, and meta
IF significantly affected body weight and intestinal morphology, compromised the intestinal barrier, increased pro-inflammatory cytokines, and heightened gut immune activation (P < 0.05). It also disrupted the gut microbiota, promoting pro-inflammatory bacteria, reducing anti-inflammatory metabolites, and elevating pro-inflammatory metabolites (P < 0.05). Indoleacrylic acid (IAA) supplementation notably alleviated intestinal inflammation and reversed immune dysfunction induced by IF (P < 0.05).
Prolonged IF exacerbates intestinal inflammation by impairing gut barrier integrity and disrupting microbial homeostasis. However, IAA supplementation effectively mitigates fasting-induced intestinal inflammation and immune imbalance, suggesting its potential as a therapeutic agent.
Core Tip: This study demonstrates that long-term intermittent fasting (IF) compromises intestinal barrier function, alters the metabolite profile (reducing anti-inflammatory compounds and increasing pro-inflammatory ones), and induces dysbiosis (increasing pathogenic bacteria while decreasing short-chain fatty acid-producing bacteria), which collectively promote Th17-driven inflammation. Exogenous indoleacrylic acid supplementation restores barrier integrity, suppresses Th17 activation, and enhances interleukin-10 expression, highlighting its therapeutic promise and emphasizing the need for a reevaluation of the long-term safety of IF due to its potential gut-disrupting effects.