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Commentary Open Access
Volume 3 | Issue 1 | DOI: https://doi.org/10.33696/genetics.3.014

Gut Microbiota Metabolite Trimethylamine N-oxide Reduced Pancreatic β Cell Calcium Transients and Function

  • 1State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
  • 2Diabetes Research Center of Chinese Academy of Medical Sciences, Beijing, China
  • 3CAMS Key Laboratory of Molecular Mechanism and Target Discovery of Metabolic Disorders and Tumorigenesis, Beijing, China
+ Affiliations - Affiliations

Corresponding Author

Pingping Li, lipp@imm.ac.cn

Received Date: May 24, 2024

Accepted Date: June 20, 2024

Abstract

Pancreatic β cell dysfunction is an important cause of type 2 diabetes (T2D). Previous studies show trimethylamine N-oxide (TMAO), a gut microbiota-related metabolite, promotes cardiovascular disease and insulin resistance. However, the effect and mechanism of TMAO at pathological concentrations on β cell function remain unknown. The recently published work demonstrates TMAO reduces pancreatic β cell function and glucose homeostasis. Furthermore, TMAO inhibits calcium transients through NLR family pyrin domain containing 3 (NLRP3) inflammasome activation and induced Serca2 loss. Additionally, long-term TMAO exposure promotes β cell endoplasmic reticulum (ER) stress, dedifferentiation and apoptosis. Here, we review the impaired effect of TMAO on β cell function and comment on the implications of this study for understanding the role and mechanism of TMAO in the development of T2D. Further work should focus on screening flavin-containing monooxygenase 3 (FMO3) inhibitors for antidiabetes.

Keywords

Trimethylamine N-oxide, Pancreatic β cell function, Calcium transients, Serca2, Antidiabetes

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