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Ruminococcus torques Administration Modestly Alleviates Dietary Selenium Deficiency-Induced Glucose Intolerance in

Ying-Chen Huang¹, Wen-Hsing Cheng²

¹Mississippi State University.

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|November 19, 2025

Summary

This summary is machine-generated.

Dietary selenium deficiency worsens type 2 diabetes symptoms in mice. Supplementing with Ruminococcus torques bacteria partially improved glucose intolerance but increased E. coli, impacting gut health and selenium-dependent proteins.

Keywords:

Ruminococcus torques Selenium deficiency glucose intolerance gut microbiota insulin resistance

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Area of Science:

Microbiome research
Nutritional science
Metabolic disease research

Background:

Dietary selenium (Se) deficiency and aging are linked to increased fecal Lachnospiraceae, including Ruminococcus torques, a bacterium associated with type 2 diabetes.
Different gut bacteria taxa have distinct effects on host physiology, necessitating a closer look at specific interactions.

Purpose of the Study:

To investigate the interaction between dietary selenium and Ruminococcus torques in the development of type 2 diabetes-like symptoms.
To determine how R. torques influences host physiology under conditions of selenium adequacy and deficiency.

Main Methods:

Female C57BL/6J mice were fed either a Se-adequate or Se-deficient diet for 26 weeks.
Ruminococcus torques was administered orally to half of the mice in each dietary group during the final 5 weeks.
Glucose tolerance, insulin resistance, fasting glucose, gut microbiota composition, and specific protein levels (SELENOP, GPX1) were assessed.

Main Results:

Selenium deficiency induced glucose intolerance and insulin resistance.
R. torques administration modestly alleviated glucose intolerance in Se-deficient mice but did not affect insulin resistance.
Se deficiency increased R. torques and E. coli abundance in the gut, with R. torques further elevating E. coli.
R. torques altered SELENOP and GPX1 protein levels in the liver, with increased GPX1 in Se-deficient mice.

Conclusions:

Ruminococcus torques partially mitigates glucose intolerance in Se-deficient mice with diabetic symptoms.
The interaction between R. torques, selenium status, and gut microbiota composition (specifically E. coli) influences host metabolic parameters.
R. torques affects selenium-dependent protein expression in the liver, highlighting a complex interplay between diet, microbiome, and host metabolism.