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

We previously found that dietary selenium (Se) deficiency and age increase the fecal abundance of Lachnospiraceae in aged telomere-humanized mice in a sexually dimorphic manner. Although Lachnospiraceae are key contributors of short-chain fatty acids to the host, different taxa within this family exert distinct effects on host physiology. Among them, Ruminococcus torques has been associated with type 2 diabetes. In the present study, we aimed to determine whether, and how, R. torques interacts with dietary Se to influence type 2 diabetes-like symptoms. Sixteen weaning female C57BL/6J mice were fed either a Se-adequate or Se-deficient diet for 26 weeks. From weeks 21 to 25, half of the mice in each dietary group received daily oral gavage of R. torques (2 × 10⁸ CFU in 0.2 mL). All mice were euthanized at week 26. Dietary Se deficiency induced glucose intolerance (13%) and insulin resistance (16%) ( P < 0.05). While R. torques administration modestly alleviated glucose intolerance in Se-deficient mice, it did not affect insulin resistance or fasting glucose levels. Se deficiency reduced the relative abundance of Lactobacillus spp ., F. prausnitzii , and Roseburia spp./E. rectale in the cecal content, and these taxa were unaffected by R. torques treatment. In contrast, Se deficiency increased the relative abundance of R. torques and E. coli in cecal samples, with E. coli levels further elevated by R. torques gavage. Notably, R. torques oral gavage 1 ) decreased SELENOP and GPX1 protein levels in the liver, but not in skeletal muscle, of Se-adequate mice; 2) increased liver GPX1 protein levels in Se-deficient mice. Altogether, R. torques administration modestly alleviates glucose intolerance and increases both liver GPX1 protein levels and cecal E. coli abundance in Se-deficient mature female mice with diabetic symptoms.