Milk Fat Globule Membrane Enhances Colonic-Mucus-Barrier Function in a Rat Model of Short-Bowel Syndrome

Zhicai Yu1, Ying Li1, Yang Niu1

  • 1Department of Clinical Nutrition, Xin Hua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Abstract

Insights

Milk fat globule membrane (MFGM) supplementation improves gut barrier function and modulates microbiota in a rat model of short-bowel syndrome (SBS). This suggests MFGM may be a promising therapeutic for SBS by strengthening the mucus barrier and regulating inflammation.

Area of Science:

  • Gastroenterology
  • Microbiology
  • Immunology

Background:

  • The colon is crucial for mitigating short-bowel syndrome (SBS) effects.
  • Milk fat globule membrane (MFGM) previously demonstrated protective effects on gut barrier integrity in a rat SBS model.

Purpose of the Study:

  • To investigate the impact of enteral MFGM supplementation on gut microbiota and colonic-mucus-barrier function in a rat SBS model.
  • To explore the underlying mechanisms, including the nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing protein 6 (NLRP6) inflammasome pathway.

Main Methods:

  • 24 male Sprague-Dawley rats were divided into Sham, SBS, and SBS+MFGM groups.
  • Evaluated gut permeability, crypt depth, goblet cells, mucins (MUC1, MUC2), microbiota, short-chain fatty acids, and NLRP6 pathway protein expressions.

Main Results:

  • SBS+MFGM rats showed reduced intestinal permeability, increased crypt depth, and more goblet cells compared to SBS rats.
  • MFGM supplementation altered gut microbiota composition, increasing Firmicutes abundance and affecting short-chain fatty acid profiles.
  • Modulation of NLRP6 inflammasome pathway components, including increased NLRP6 and IL-18, and decreased IL-1β and Caspase-1 expression was observed in the SBS+MFGM group.

Conclusions:

  • Enteral MFGM supplementation modulates gut microbiota in SBS.
  • MFGM may strengthen the colonic mucus barrier and regulate the NLRP6 inflammasome, offering a potential therapeutic strategy for SBS.