Previous obesity in mice can lead to epigenetic changes

The obesity previous can trigger epigenetic changes persistent in innate immunity and neuroinflammationaccording to a study conducted in mice published by Science Advances.

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A history of obesity caused by a high-fat diet produces changes in innate immunity that may promote inflammatory diseaseschanges that persist even after losing weight and returning to a normal metabolism, the research notes.

If these findings translate to humans, the authors suggest that these epigenetic changes could contribute to predisposition to age-related and obesity-associated neuroinflammatory diseases.

Age-related macular degeneration, a neuroinflammatory disease and the main cause of irreversible blindness in the elderly, has been linked to obesity; however, the mechanisms by which obesity predisposes to suffering from it are not well defined.

The long-term impact of prior obesity on the immune response later in life is also unknown.

The team led by researchers from the University of Montreal (Canada) carried out a series of experiments with mice.

In them they saw that the adipose tissue macrophages Mice fed a high-fat diet exhibited epigenetic changes that lead to increased expression of genes involved in inflammatory responses.

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That gene expression continued after the rodents returned to their normal weight and metabolic normalcy.

The persistent epigenetic changes occurred during a period of obesity in which fatty acids such as steric acid altered resident macrophages in adipose tissue towards a proinflammatory phenotype, which is maintained during ageing.

These resident inflammatory cells can travel to other parts of the body, including the eye, where they initiate an inflammatory program that promotes age-related macular degeneration.

In a commentary published by Science Advances related to the study, Kevin Mangum and Katherine Gallagher of the University of Michigan, who were not involved in the research, stress that it raises “important questions.”

In this sense, they refer to the previous pathways responsible for epigenetic reprogramming in macrophages and whether their treatment can reverse the epigenetic changes.

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