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Magnesium (Mg) deficiency is a common nutritional disorder that is linked to an inflammatory state characterized by increased plasma acute phase protein and proinflammatory cytokine concentrations. Recent studies have shown that changes in the composition of gut microbiota composition participate in systemic inflammation. In this study, therefore, we assessed the potential role of gut microbiota in intestinal and systemic inflammation associated with Mg deficiency in mice. For this purpose, mice were fed a control or Mg-deficient diet (500 mg vs. 70 mg Mg/kg) for 4 or 21 d. Compared with the mice fed the control diet, mice fed the Mg-deficient diet for 4 d had a lower gut bifidobacteria content (-1.5 log), a 36-50% lower mRNA content of factors controlling gut barrier function in the ileum (zonula occludens-1, occludin, proglucagon), and a higher mRNA content (by approximately 2-fold) in the liver and/or intestine of tumor necrosis factor-alpha, interleukin-6, CCAAT/enhancer binding protein homologous protein, and activating transcription factor 4, reflecting inflammatory and cellular stress. In contrast, mice fed the Mg-deficient diet for 21 d had a higher cecal bifidobacteria content compared with the control group, a phenomenon accompanied by restoration of the intestinal barrier and the absence of inflammation. In conclusion, we show that Mg deficiency, independently of any other changes in nutrient intake, modulates the concentration of bifidobacteria in the gut, a phenomenon that may time-dependently affect inflammation and metabolic disorders in mice.
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http://dx.doi.org/10.3945/jn.109.117374 | DOI Listing |
Life Sci
September 2025
Department of Experimental Medical Science, Faculty of Medicine, Lund University, 221 84, Lund, Sweden; Wallenberg Center for Molecular Medicine, Faculty of Medicine, Lund University, 221 84, Lund, Sweden. Electronic address:
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September 2025
Laboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka 565-0871, Japan. Electronic address:
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September 2025
Guizhou Medical University, Guiyang 550004 Guizhou, PR China; Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang 550004 Guizhou, PR China; The Key Laboratory of Myocardial Remodeling Research, The Affiliated Hospital of Guizhou Medical University, G
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Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. Electronic address:
Diet and obesity contribute to insulin resistance and type 2 diabetes, in part via the gut microbiome. To explore the role of gut-derived metabolites in this process, we assessed portal/peripheral blood metabolites in mice with different risks of obesity/diabetes, challenged with a high-fat diet (HFD) + antibiotics. In diabetes/obesity-prone C57BL/6J mice, 111 metabolites were portally enriched and 74 were peripherally enriched, many of which differed in metabolic-syndrome-resistant 129S1/129S6 mice.
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Department of Hepatology, Center of Infectious Diseases and Pathogen Biology, the First Hospital of Jilin University, Changchun, China; Jilin Provincial Key Laboratory of Metabolic Liver Diseases, Jilin University, Changchun, China; China-Singapore Belt and Road Joint Laboratory on Liver Disease Res
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