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Intestinal stem cells (ISCs) remember high-fat diet (HFD) exposure through lasting epigenetic changes in their chromatin. This dietary memory influences ISC self-renewal and adenoma growth, even after returning to a normal diet.

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Area of Science:

  • Cell Biology
  • Epigenetics
  • Metabolism

Background:

  • Intestinal stem cells (ISCs) respond to dietary signals via metabolic and transcriptional pathways.
  • The long-term epigenetic consequences of dietary intake on ISCs are not well understood.

Purpose of the Study:

  • To investigate how a high-fat diet (HFD) induces lasting epigenetic modifications in ISCs.
  • To determine if these diet-induced chromatin changes persist and affect ISC function and tumor development.

Main Methods:

  • Utilized a high-fat Western diet (HFD) mouse model.
  • Analyzed chromatin accessibility changes in ISCs and their differentiated progeny.
  • Examined the role of PPAR-delta/alpha nuclear receptors and APC tumor suppressor in diet-induced epigenetic alterations.

Main Results:

  • HFD broadly remodels chromatin accessibility in ISCs, creating differentially accessible regions (DARs).
  • HFD-induced DARs persist through ISC differentiation and even after diet normalization.
  • These epigenetic changes enhance ISC self-renewal and adenoma growth upon re-exposure to HFD.
  • HFD-induced chromatin changes depend on PPAR-delta/alpha but not their direct transcriptional targets.
  • Tumor suppressor APC inactivation overrides diet-dependent chromatin changes in Lgr5+ ISCs.

Conclusions:

  • ISCs retain a stable, chromatin-based memory of dietary fat exposure.
  • This epigenetic memory influences ISC behavior and susceptibility to tumor formation.
  • Dietary fat impacts intestinal epigenetics, with implications for stem cell function and cancer.