High-fat diet may be physically changing the liver

MIT researchers reported that long-term high-fat diets in mice shifted liver cells from normal metabolic and detoxifying roles to stress‑survival programs associated with tumor development, and similar declines in normal liver activity were observed in human samples; the study was largely in mice, so human implications remain uncertain.

Researchers at the Massachusetts Institute of Technology reported that long-term high-fat diets in mice changed the behavior of liver cells, moving them away from normal metabolic and detoxifying roles toward stress‑survival programs. The work, published in Cell, tracked those cellular changes as some mice later developed liver cancer. Human liver samples showed comparable declines in normal activity, but the study did not follow people over time to measure cancer outcomes. Key findings: - In mice, repeated exposure to a high-fat diet led liver cells to reduce normal functions and adopt survival-oriented gene programs linked to tumorigenesis. - Some mice fed long-term high-fat diets went on to develop liver cancer, and researchers observed the cell-state changes during disease progression. - Human liver samples showed similar declines in normal liver activity, though the study did not track long-term cancer outcomes in people. - The research team noted the findings are largely based on mouse models and early genetic changes and do not fully account for factors such as insulin resistance, inflammation, or alcohol use. Summary: The study offers a biological explanation for how prolonged exposure to high dietary fat might precede fatty liver disease and later contribute to cancer-related cellular changes, with mice showing the process over about a year and researchers estimating it could take decades in humans. The team plans further research to see whether changes in eating patterns or medications being studied for weight loss could restore normal liver cell behavior; broader implications for people remain undetermined at this time.