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<p>We previously found that dietary selenium (Se) deficiency and age increase the fecal abundance of <i>Lachnospiraceae</i> in aged telomere-humanized mice in a sexually dimorphic manner. Although <i>Lachnospiraceae</i> are key contributors of short-chain fatty acids to the host, different taxa within this family exert distinct effects on host physiology. Among them, <i>Ruminococcus torques</i> has been associated with type 2 diabetes. In the present study, we aimed to determine whether, and how, <i>R. torques</i> 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 <i>R. torques</i> (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%) (<i>P</i> &lt; 0.05). While <i>R. torques</i> administration was associated with a reduction in glucose levels at 30&#xa0;min post-injection in Se-deficient mice, it did not significantly alter the overall glucose area under the curve, insulin resistance, or fasting glucose levels. Se deficiency reduced the relative abundance of <i>Lactobacillus spp</i>., <i>F. prausnitzii</i>, and <i>Roseburia spp./E. rectale</i> in the cecal content, and these taxa were unaffected by <i>R. torques</i> treatment. In contrast, Se deficiency increased the relative abundance of <i>R. torques</i> and <i>E. coli</i> in cecal samples, with <i>E. coli</i> levels further elevated by <i>R. torques</i> gavage. Notably, <i>R. torques</i> oral gavage <i>1</i>) decreased SELENOP and GPX1 protein levels in the liver, but not in skeletal muscle, of Se-adequate mice; <i>2)</i> increased liver GPX1 protein levels in Se-deficient mice. Altogether, <i>R. torques</i> administration exerts a marginal effect on glucose excursion and increases both liver GPX1 protein levels and cecal <i>E. coli</i> abundance in Se-deficient mature female mice with diabetic symptoms.</p>

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Impact of Ruminococcus torques Administration on Glucose Tolerance and Hepatic Selenoprotein Expression in Selenium-deficient Mature Female Mice

  • 期刊论文

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  • 发表日期：

    2026年5月13日

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  • Ying-Chen Huang,
  • Wen-Hsing Cheng

摘要

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 was associated with a reduction in glucose levels at 30 min post-injection in Se-deficient mice, it did not significantly alter the overall glucose area under the curve, 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 exerts a marginal effect on glucose excursion and increases both liver GPX1 protein levels and cecal E. coli abundance in Se-deficient mature female mice with diabetic symptoms.