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B3galt5 functions as a PXR target gene and regulates obesity and insulin resistance by maintaining intestinal

Jinhang Zhang1, Ya Huang1,2, Hong Li1

  • 1Department of Pharmacy, Institute of Metabolic Diseases and Pharmacotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.

Nature Communications
|July 14, 2024
PubMed

Insights

Intestinal Pregnane X receptor (PXR) activation improves obesity by upregulating B3GALT5, which maintains gut barrier integrity. This highlights intestinal PXR as a therapeutic target for metabolic homeostasis.

Area of Science:

  • Metabolic disease research
  • Gastroenterology
  • Pharmacology

Background:

  • Intestinal barrier dysfunction is linked to metabolic disorders.
  • The role of intestinal Pregnane X receptor (PXR) in metabolic diseases is largely unknown.

Purpose of the Study:

  • To investigate the role of intestinal PXR in high fat diet (HFD)-induced obesity.
  • To explore the therapeutic potential of intestinal PXR activation.

Main Methods:

  • Activation of PXR using tributyl citrate (TBC), an intestinal-selective agonist.
  • Analysis of B3GALT5 expression and its role in HFD-induced obesity.
  • Assessment of intestinal barrier integrity and mucin O-glycosylation.

Main Results:

  • Intestinal PXR activation by TBC ameliorates HFD-induced obesity.
  • B3GALT5 is a direct PXR target gene crucial for intestinal mucus barrier integrity.
  • B3GALT5 deficiency exacerbates obesity, insulin resistance, and inflammation, abolishing TBC's benefits.

Conclusions:

  • Intestinal PXR activation improves metabolic homeostasis by upregulating B3GALT5.
  • B3GALT5 maintains intestinal barrier function through mucin O-glycosylation.
  • Intestinal-selective PXR activation is a potential therapeutic strategy for obesity.

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