<i>Anaerobutyricum soehngenii</i> Reduces Hepatic Lipogenic Pathways and Increases Intestinal Gluconeogenic Gene Expression in Metabolic-Dysfunction-Associated Steatotic Liver Disease (MASLD) Mice

oleh: Anne Linde Mak, Quinten J. J. Augustijn, Clément J. F. Heymann, Stefan Havik, Xanthe Verdoes, Melany Rios-Morales, Laura A. Bosmans, Joanne Verheij, Abraham S. Meijnikman, Patrick A. de Jonge, Hilde Herrema, Willem M. de Vos, Max Nieuwdorp, Aldo Grefhorst, Adriaan G. Holleboom

Format: Article
Diterbitkan: MDPI AG 2024-03-01

Deskripsi

Metabolic-dysfunction-associated steatotic liver disease (MASLD) is a growing health problem for which no therapy exists to date. The modulation of the gut microbiome may have treatment potential for MASLD. Here, we investigated <i>Anaerobutyricum soehngenii</i>, a butyrate-producing anaerobic bacterium with beneficial effects in metabolic syndrome, in a diet-induced MASLD mouse model. Male C57BL/6J mice received a Western-type high-fat diet and water with 15% fructose (WDF) to induce MASLD and were gavaged with <i>A. soehngenii</i> (10<sup>8</sup> or 10<sup>9</sup> colony-forming units (CFU) 3 times per week) or a placebo for 6 weeks. The <i>A. soehngenii</i> gavage increased the cecal butyrate concentrations. Although there was no effect on histological MASLD scores, <i>A. soehngenii</i> improved the glycemic response to insulin. In the liver, the WDF-associated altered expression of three genes relevant to the MASLD pathophysiology was reversed upon treatment with <i>A. soehngenii</i>: Lipin-1 (<i>Lpin1</i>), insulin-like growth factor binding protein 1 (<i>Igfbp1</i>) and Interleukin 1 Receptor Type 1 (<i>Il1r1</i>). <i>A. soehngenii</i> administration also increased the intestinal expression of gluconeogenesis and fructolysis genes. Although these effects did not translate into significant histological improvements in MASLD, these results provide a basis for combined gut microbial approaches to induce histological improvements in MASLD.