Document Type

Article

Publication Date

2023

Publisher

Elsevier

Source Publication

Cellular and Molecular Gastroenterology and Hepatology (CMGH)

Source ISSN

2352-345X

Original Item ID

DOI: 10.1016/j.jcmgh.2023.05.001

Abstract

Background & Aims

The colonic epithelium requires continuous renewal by crypt resident intestinal stem cells (ISCs) and transit-amplifying (TA) cells to maintain barrier integrity, especially after inflammatory damage. The diet of high-income countries contains increasing amounts of sugar, such as sucrose. ISCs and TA cells are sensitive to dietary metabolites, but whether excess sugar affects their function directly is unknown.

Methods

Here, we used a combination of 3-dimensional colonoids and a mouse model of colon damage/repair (dextran sodium sulfate colitis) to show the direct effect of sugar on the transcriptional, metabolic, and regenerative functions of crypt ISCs and TA cells.

Results

We show that high-sugar conditions directly limit murine and human colonoid development, which is associated with a reduction in the expression of proliferative genes, adenosine triphosphate levels, and the accumulation of pyruvate. Treatment of colonoids with dichloroacetate, which forces pyruvate into the tricarboxylic acid cycle, restored their growth. In concert, dextran sodium sulfate treatment of mice fed a high-sugar diet led to massive irreparable damage that was independent of the colonic microbiota and its metabolites. Analyses on crypt cells from high-sucrose–fed mice showed a reduction in the expression of ISC genes, impeded proliferative potential, and increased glycolytic potential without a commensurate increase in aerobic respiration.

Conclusions

Taken together, our results indicate that short-term, excess dietary sucrose can directly modulate intestinal crypt cell metabolism and inhibit ISC/TA cell regenerative proliferation. This knowledge may inform diets that better support the treatment of acute intestinal injury.

Comments

Accepted version. Cellular and Molecular Gastroenterology and Hepatology (CMGH), Vol. 16, No. 2 (2023): 287-316. DOI. © 2023 Elsevier. Used with permission.

Marshall_16185acc.docx (2783 kB)
ADA Accessible Version

Included in

Biology Commons

Share

COinS