メイヨー・クリニックの研究者らは、世界中の成人の約3分の1に影響を及ぼす代謝機能異常関連脂肪肝疾患を直接引き起こす稀なMET遺伝子変異を発見した。この知見は、典型的なリスクファクターがない家族例に基づいており、同様の変異が多くの他の人々の疾患に寄与している可能性を示唆している。Hepatology誌に掲載されたこの研究は、ゲノム解析が隠れた遺伝的原因を明らかにする役割を強調している。
メイヨー・クリニック個別化医療センターの科学者らは、以前は非アルコール性脂肪肝疾患として知られていた代謝機能異常関連脂肪肝疾患（MASLD）を引き起こす稀なMET遺伝子の遺伝子変異を特定した。MET遺伝子は肝臓の修復と脂肪処理に重要であり、変異すると肝細胞に脂肪が蓄積し、炎症、線維化、瘢痕化が生じ、最終的に肝硬変や肝がんに至る可能性がある。
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Researchers in Barcelona report that the lipid drug pemafibrate and the blood-pressure medicine telmisartan reduced diet-induced liver fat in rats and in a zebrafish model of fatty liver disease, with a half-dose combination performing as well as full doses of either drug alone. The work, published in Pharmacological Research, also describes a role for the PCK1 protein in telmisartan’s liver effects and argues that clinical trials would be needed to confirm any benefit in people.
Researchers at the University of Adelaide have found that blocking the enzyme Caspase-2, previously seen as a potential treatment for fatty liver disease, may increase the risk of chronic liver damage and cancer over time. In genetically modified mice lacking functional Caspase-2, liver cells grew abnormally large and accumulated genetic damage, leading to inflammation, scarring, and tumors. The findings, published in Science Advances, challenge the development of Caspase-2 inhibitors.
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Researchers at UCLA have identified senescent immune cells, dubbed 'zombie' cells, that accumulate in aging livers and contribute to fatty liver disease. By eliminating these cells in mice, the team reversed liver damage and reduced body weight, even on an unhealthy diet. The findings, published in Nature Aging, suggest similar mechanisms may drive human liver conditions.
Researchers have uncovered links between microbes in the mouth and metabolic conditions like obesity, pre-diabetes, and fatty liver disease. The study analyzed oral swabs from over 9,000 participants using advanced sequencing techniques. Experts suggest these findings could lead to simple swab-based screenings.
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A new genomic analysis suggests that Alzheimer's disease may begin with inflammation in organs like the skin, lungs, or gut, potentially decades before brain symptoms appear. Researchers analyzed genetic data from hundreds of thousands of people and found risk genes more active outside the brain. This perspective could reshape prevention and treatment strategies.