Fats, immunity and aging: what the ELOVL2 enzyme is hiding
As we age, our immunity declines, but why this happens has long been a mystery. A discovery by American biologists has shown that the key to the weakening of the body’s defenses may lie in one small enzyme responsible for lipids – the fats on which immune cells depend.
As we age, it becomes increasingly difficult for the body to defend itself against disease. Immune cells are produced worse, react slower, and recovery from simple inflammations takes longer. Why this happens is a question that experts have long puzzled over.
A recent publication in the journal GeroScience points to an unexpected reason: the key factor may be an enzyme with a difficult name – ELOVL2. It is involved in the production of fatty acids, without which the normal development of immune cells, in particular B-lymphocytes – they are responsible for the production of antibodies.
A team from the University of California, San Diego and Irvine found that the activity of ELOVL2 decreases with age. Once this enzyme becomes scarce, the ratio of saturated to unsaturated fats in cells changes, which disrupts their structure and makes it impossible for immune cells to develop.
In experiments on mice, it was shown that animals with the ELOVL2 gene “turned off” aged much faster at the cellular level. In the bone marrow of such individuals, scientists noticed a sharp drop in the activity of genes associated with immune defense. Moreover, the fat profile of their cells resembled older animals, even if they were only 18 months old.
Interestingly, the pattern appeared similar in humans as well. In bone marrow samples from people over 60 years of age, cells containing ELOVL2 practically disappeared. In parallel, the activity of the CD79B gene – one of the most important for the immune response – decreased.
But it’s not just about immunity. According to scientists, the violation of fat metabolism affects other important processes in the body. Lack of omega-3 acids, especially DHA, disrupts the flexibility and strength of cell membranes, which affects the “endurance” of cells. When ELOVL2 is deficient, membranes lose elasticity, which is especially critical for B-lymphocyte progenitor cells.
One of the authors of the study emphasizes: the normal diet is not able to compensate for the decrease in ELOVL2. Foods with insufficient amounts of healthy fats, especially omega-3, can only accelerate the aging of the immune system.
The way out may lie in point lipid support – supplements tailored to the body’s individual needs. However, scientists warn: before such preparations appear in pharmacies, it is necessary to find out how exactly and in what form to deliver fatty acids so that they are not destroyed in the stomach.
The discovery also opens new horizons in the fight against blood cancers. Genes regulated by ELOVL2 are often linked to the development of diseases such as lymphoma and myeloma. Scientists suggest that interfering with fat metabolism may slow the progression of cancer cells.
The researchers are confident: by studying the aging process, it is possible to find not only ways to extend active life, but also new approaches to the treatment of age-related diseases and cancer.
Published
April, 2025
Duration of reading
3-4 minutes
Category
Science
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