The global prevalence of metabolic diseases is on the increase, and it has become a significant threat to the health and lives of individuals. Ergothioneine (EGT) is a natural betaine amino acid found in various foods, particularly mushrooms. EGT cannot be synthesized by mammals; it is absorbed into small intestinal epithelial cells by a cationic protein, the novel organic cation transporter 1 (OCTN1), and transported to certain organs. Consistent with its structure, EGT has been reported to exhibit antioxidant, anti-inflammatory, anti-apoptotic, anti-aging, and metal-chelating effects. The unique chemical properties and biological functions of EGT position it as a promising candidate for the research and treatment of metabolic diseases. This review summarizes EGT's capacities, potential therapeutic effects on multiple metabolic diseases, and their specific mechanisms. Finally, we outline challenges for future research on EGT and aspire to establish it as a prospective therapeutic agent for metabolic diseases.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.jnutbio.2025.109895 | DOI Listing |
JMIR Res Protoc
March 2025
Institute for Data Science and Informatics, University of Missouri, Columbia, MO, United States.
Background: Amyotrophic lateral sclerosis (ALS) leads to rapid physiological and functional decline before causing untimely death. Current best-practice approaches to interdisciplinary care are unable to provide adequate monitoring of patients' health. Passive in-home sensor systems enable 24×7 health monitoring.
View Article and Find Full Text PDFPLoS One
March 2025
Public Health Research Center, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates.
Introduction: Family history of cardiovascular disease (CVD) is an independent risk factor for coronary heart disease, and the risk increases with number of family members affected. It offers insights into shared genetic, environmental and lifestyle factors that influence heart disease risk. In this study, we aimed to estimate the association of family history of CVD and its risk factors, as well as the number of affected parents or siblings, with the prevalence of major cardiometabolic risk factors (CRFs) such as hypertension, dysglycemia, dyslipidemia and obesity in a sample of young adults.
View Article and Find Full Text PDFHealth Syst Reform
December 2025
Department of Obstetrics and Gynecology, University of Benin, Nigeria.
Diabetes mellitus, once a rare diagnosis in precolonial and early post-colonial Nigeria, now has the highest prevalence and fatality rates in sub-Saharan Africa. This increased prevalence is attributed to rising population affluence characterized by sedentary lifestyles and higher consumption of processed and ultra-processed foods. The burden is further exacerbated by a poorly responsive healthcare system.
View Article and Find Full Text PDFJ Immunol
January 2025
Center for Translational Immunology, Benaroya Research Institute, Seattle, WA, United States.
The CD2-depleting drug alefacept (LFA3-Ig) preserved beta cell function in new-onset type 1 diabetes (T1D) patients. The most promising biomarkers of response were late expansion of exhausted CD8 T cells and rare baseline inflammatory islet-reactive CD4 T cells, neither of which can be used to measure responses to drug in the weeks after treatment. Thus, we investigated whether early changes in T cell immunophenotypes could serve as biomarkers of drug activity.
View Article and Find Full Text PDFJ Immunol
January 2025
Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA, United States.
Macrophages are critical to maintaining and restoring tissue homeostasis during inflammation. The lipid metabolic state of macrophages influences their function and polarization, which is crucial to the resolution of inflammation. The contribution of lipid synthesis to proinflammatory macrophage responses is well understood.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!