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Related Concept Videos

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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Related Experiment Video

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Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
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Ketone ester supplementation protects from experimental colitis via improved goblet cell differentiation and

Nadine Rohwer1,2,3, Anika Sander4,5, Soeren Ocvirk4,5

  • 1Medical Department B, Division of Hepatology, Gastroenterology, Oncology, Hematology, Palliative Care, Endocrinology and Diabetes, Brandenburg Medical School, University Hospital Ruppin-Brandenburg, Neuruppin, Germany.

European Journal of Nutrition
|November 12, 2025
PubMed
Summary

Ketone esters (KE) effectively reduced intestinal inflammation in mouse models of colitis, unlike ketogenic diets (KD). KE supplementation enhanced the mucus barrier and beneficial gut bacteria, suggesting therapeutic potential for inflammatory bowel disease.

Keywords:
ColitisGoblet cellInflammatory bowel diseaseKetogenic dietKetone esterMicrobiome

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Area of Science:

  • Gastroenterology
  • Nutrition Science
  • Microbiology

Background:

  • Ketogenic diets (KD) and ketone bodies show therapeutic promise but their role in inflammatory bowel diseases (IBD) is debated.
  • Ketone esters (KE) offer an ingestible source of ketone bodies.

Purpose of the Study:

  • To investigate the effects of KD and KE on intestinal inflammation in murine colitis models.
  • To compare the impact of KD feeding versus KE supplementation on the gut mucus barrier and microbiota composition.

Main Methods:

  • Utilized acute dextran sodium sulfate (DSS) and 2,4,6-trinitrobenzene sulfonic acid (TNBS) induced murine colitis models.
  • Assessed colitis activity, colonic mucus barrier integrity (mucin2 expression, goblet cell differentiation), and gut microbiota composition (16S rRNA sequencing).

Main Results:

  • KD feeding did not significantly alter colitis activity.
  • KE supplementation alleviated colitis, enhancing mucin2 expression and goblet cell differentiation.
  • KE increased the abundance of mucus-degrading Akkermansia, a key gut commensal.

Conclusions:

  • KE show potential as an anti-inflammatory dietary supplement for acute colitis.
  • KE may exert therapeutic effects by modulating mucin2, goblet cell function, and Akkermansia abundance.
  • Further research is warranted to explore KE's therapeutic role in inflammatory bowel disease.