Mechanisms Underlying the Effects of Edible Mushrooms on Gastrointestinal Health

Open Access
Roy, Pratiti
Area of Honors:
Biochemistry and Molecular Biology
Bachelor of Science
Document Type:
Thesis Supervisors:
  • Margherita Teresa-Anna Cantorna, Thesis Supervisor
  • Ming Tien, Honors Advisor
  • Andrew David Patterson, Faculty Reader
  • Mushrooms
  • Intestinal gluconeogenesis
  • gut microbiota
  • gut-brain neural circuit
White button (WB) mushrooms (Agaricus bisporus) have been shown to promote gastrointestinal health and protect the gastrointestinal tract from infection and injury. The protection provided by mushrooms is thought to be linked to the microbiota. The goal of this project was to look into the mechanism underlying this effect and to characterize the effect of mushrooms on the gut microbiota. One group of mice (n=7) was fed WB diet (1%) every day for 2 weeks. The control group (n=7) was fed the control (CTRL) diet. 1H NMR analysis of the cecal contents showed higher levels of the metabolite succinate. When the same experiment was run in germ-free (GF) mice (mice that are free from microorganisms), succinate was not found in the cecum. Furthermore, microbial DNA was extracted from cecal contents and analyzed via qPCR, showing increased levels of the succinate-producing bacteria Prevotella in WB treated mice. This suggests that the succinate found in conventional (CV), WB-fed mice is a microbial product. Increased levels of succinate have been linked to improved glucose homeostasis via intestinal gluconeogenesis (IGN). The results from our experiment confirmed this, there were significantly higher levels of mRNA encoding for the IGN-related enzymes Glut2 and G6Pase in the jejunum of WB-fed mice. In addition to this, expression of two genes involved in energy homeostasis, Sglt3 and Ffar3, was also found to be significantly elevated in WB-fed mice. A potential mechanism of WB mushroom protection is through an increase in succinate-producing bacteria. This could contribute to improved glucose homeostasis through IGN, which is regulated via receptors like FFAR3 and SGLT3, which provide a connection between the gut and the nervous system.