Metabolite mimicry identifies butyrate analogs with select protective functions in the intestinal mucosa

A Alfredo Ornelas (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) J Jacob A. Countess (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) J Ji Yeon Kim (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) R Rachel H. Cohen (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) B Brittany D. Gomez (Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Colorado Anschutz Medical Campus) R Rebecca L. Roer (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) F Faiz Minhajuddin (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) K Kiranmayee Yenugudhati Vijaya Sai (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) L Liheng Zhou (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) J Julia L. M. Dunn (Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Colorado Anschutz Medical Campus) C Caleb Chandler (Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus) P Philip Reigan (Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus) I Ian M. Cartwright (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) C Caroline H. T. Hall (Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Colorado Anschutz Medical Campus) G Geetha Bhagavatula (Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Colorado Anschutz Medical Campus) J Joseph C. Onyiah (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) A Alexander S. Dowdell (Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus) S Sean P. Colgan (Mucosal Inflammation Program, Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus)

Abstract

Microbial-derived short-chain fatty acids regulate a variety of pathways in the healthy colonic mucosa. In particular, butyrate serves as the primary energy source for colonocytes and regulates gene transcription by stabilizing the transcription factor hypoxia-inducible-factors (HIF) and functioning as a histone deacetylase (HDAC) inhibitor. A limitation of butyrate as a therapeutic is its rapid metabolism in differentiated colonocytes. Furthermore, intestinal stem cells (ISCs) respond differently to butyrate, preferentially using glucose for energy procurement. To address these limitations, we explored metabolite mimicry to identify compounds with potent or selective biological responses within the butyrate pathway(s). We found an analog, 3-chlorobutyrate (3-Cl BA), that significantly enhances epithelial barrier formation and wound healing in vitro. Mechanistically, we revealed that 3-Cl BA is a potent HDAC inhibitor. Furthermore, unlike butyrate, 3-Cl BA does not stabilize HIF and it is not used as metabolic fuel. In vivo studies in a dextran sulfate sodium-colitis model revealed that contrary to butyrate, 3-Cl BA is protective. Studies in stem-like colonoids demonstrated that only butyrate inhibits ISC proliferation and differentiation. Furthermore, it was recently reported that HIF stabilization inhibits ISCs activity. Given the fact that butyrate but not 3-Cl BA stabilizes HIF, we surmised that 3-Cl BA would circumvent these detrimental functional consequences. We demonstrate here that pharmacologic HIF stabilization inhibits colonoid differentiation and that genetic loss of HIF significantly promotes ISC differentiation. This study reveals a promising butyrate analog protective in colitis and demonstrates the advantages of metabolite mimicry to dissect selective biological functions from major metabolites in the gut.

Article Details

Volume / Issue Vol. 123, Issue 15
Published April 14, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (18)

A

Alfredo Ornelas

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

J

Jacob A. Countess

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

J

Ji Yeon Kim

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

R

Rachel H. Cohen

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

B

Brittany D. Gomez

Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Colorado Anschutz Medical Campus

R

Rebecca L. Roer

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

F

Faiz Minhajuddin

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

K

Kiranmayee Yenugudhati Vijaya Sai

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

L

Liheng Zhou

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

J

Julia L. M. Dunn

Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Colorado Anschutz Medical Campus

C

Caleb Chandler

Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus

P

Philip Reigan

Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus

I

Ian M. Cartwright

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

C

Caroline H. T. Hall

Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Colorado Anschutz Medical Campus

G

Geetha Bhagavatula

Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Colorado Anschutz Medical Campus

J

Joseph C. Onyiah

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

A

Alexander S. Dowdell

Mucosal Inflammation Program and Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus

S

Sean P. Colgan

Mucosal Inflammation Program, Division of Gastroenterology and Hepatology, Department of Medicine, University of Colorado Anschutz Medical Campus