Bisphenol S exposure affects gene expression related to intestinal glucose absorption and glucose metabolism in mice

Environ Sci Pollut Res Int. 2019 Feb;26(4):3636-3642. doi: 10.1007/s11356-018-3823-z. Epub 2018 Dec 7.


Bisphenol S, an industrial chemical, has raised concerns for both human and ecosystem health. Yet, health hazards posed by bisphenol S (BPS) exposure remain poorly studied. Compared to all tissues, the intestine and the liver are among the most affected by environmental endocrine disruptors. The aim of this study was to investigate the molecular effect of BPS on gene expression implicated in the control of glucose metabolism in the intestine (apelin and its receptor APJ, SGLT1, GLUT2) and in the liver (glycogenolysis and/or gluconeogenesis key enzymes (glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK)) and pro-inflammatory cytokine expression (TNF-α and IL-1β)). BPS at 25, 50, and 100 μg/kg was administered to mice in water drink for 10 weeks. In the duodenum, BPS exposure reduces significantly mRNA expression of sodium glucose transporter 1 (SGLT1), glucose transporter 2 (GLUT2), apelin, and APJ mRNA. In the liver, BPS exposure increases the expression of G6Pase and PEPCK, but does not affect pro-inflammatory markers. These data suggest that alteration of apelinergic system and glucose transporters expression could contribute to a disruption of intestinal glucose absorption, and that BPS stimulates glycogenolysis and/or gluconeogenesis in the liver. Collectively, we reveal that BPS heightens the risk of metabolic syndrome.

Keywords: Apelinergic system; Bisphenol S; Glucose transporters (SGLT1/GLUT2); Health hazards; Intestinal glucose absorption.

MeSH terms

  • Animals
  • Apelin / genetics
  • Apelin / metabolism
  • Apelin Receptors / genetics
  • Apelin Receptors / metabolism
  • Gene Expression Regulation / drug effects*
  • Gluconeogenesis / drug effects
  • Gluconeogenesis / genetics
  • Glucose / genetics*
  • Glucose / metabolism
  • Glucose Transporter Type 2 / genetics
  • Glucose Transporter Type 2 / metabolism
  • Glucose-6-Phosphatase / genetics
  • Interleukin-1beta / metabolism
  • Intestinal Absorption / drug effects*
  • Intestinal Absorption / genetics
  • Intestines / drug effects
  • Intestines / physiology
  • Liver / drug effects
  • Liver / physiology
  • Male
  • Mice
  • Phenols / toxicity*
  • Sodium-Glucose Transporter 1 / genetics
  • Sodium-Glucose Transporter 1 / metabolism
  • Sulfones / toxicity*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism


  • Apelin
  • Apelin Receptors
  • Apln protein, mouse
  • Aplnr protein, mouse
  • Glucose Transporter Type 2
  • IL1B protein, mouse
  • Interleukin-1beta
  • Phenols
  • Slc2a2 protein, mouse
  • Slc5a1 protein, mouse
  • Sodium-Glucose Transporter 1
  • Sulfones
  • Tumor Necrosis Factor-alpha
  • bis(4-hydroxyphenyl)sulfone
  • Glucose-6-Phosphatase
  • Glucose