Ionizing Radiation and High-Fat Diet: Risk for Insulin Resistance and Epigenetic Changes

What is it about?

The study investigates the effects of ionizing radiation on the risk of insulin resistance and metabolic disorders in mice fed a high-fat diet. The results show that exposure to ionizing radiation reprograms the epigenome of skeletal muscle and fat progenitor cells, specifically affecting genes controlling the cell cycle, metabolism, and epigenetic modifiers. This leads to disturbances in the growth homeostasis of these tissues and increases the risk of metabolic disease after cancer treatment. The study provides insight into the mechanisms by which ionizing radiation affects progenitor cells and impairs their capacity to differentiate, contributing to long-term side effects of radiation on metabolic health.

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Why is it important?

This research is important because it provides insight into the mechanisms by which exposure to ionizing radiation affects skeletal muscle and adipose progenitor cells, leading to impaired metabolism and increased risk of chronic metabolic disorders such as insulin resistance and type 2 diabetes later in life. Key Takeaways: 1. Ionizing radiation increases the risk for insulin resistance in mice fed an HFD and disturbs growth homeostasis of fat and skeletal muscle in mice fed an HFD. 2. Exposure to ionizing radiation reprograms the epigenome of skeletal muscle and fat progenitor cells, specifically at genes controlling the cell cycle, metabolism, and epigenetic modifiers. 3. Epigenetic changes in peripheral tissues controlling glucose homeostasis and body mass may influence the risk for metabolic disease after cancer treatment. 4. Ionizing radiation potentiates insulin-stimulated ERK signaling, which occurs in both skeletal muscle and fat progenitors, and could be a mechanism by which ionizing radiation induces peripheral insulin resistance. 5. Ionizing radiation remodels the epigenome of skeletal muscle and fat progenitor cells, potentially through DNA damage, induces epigenetic remodeling through the regulation of epigenetic modifiers.