LIPOTOXICITY AND CELLULAR DAMAGE: CONTRIBUTION OF LIPOGENESIS ASSOCIATED WITH THE CONSU MPTION OF ULTRA -PROCESSED FOODS AND SEDENTARY BEHAVIOR

Resumo

The increasing consumption of ultra -processed foods, combined wit h the increase in sedentary behavior, has become a significant public health issue, contributing substantially to the development of chronic non-communicable diseases, such as obesity, type 2 diabetes mellitus and metabolic syndrome. These factors promote imbalances between synthesis and lipid oxidation, favoring fat deposition in non -adipose tissues, triggering lipotoxicity, mitochondrial dysfunction and progressive cell damage. This process triggers mitochondrial dysfunction, oxidative stress, chronic inflammation and progressive cell damage, consolidating itself as a central mechanism in metabolic pathophysiology. The present study aimed to analyze how the consumption of ultra - processed foods and sedentary behavior contribute to lipotoxicity and cell dama ge. This is a narrative literature review carried out through searches in the PubMed and SciELO databases. The following descriptors were used: "ultra -processed foods", "sedentary behavior", "lipogenesis", "lipotoxicity" and "cellular damage", combined thr ough Boolean operators (AND). Articles published between 2020 and 2026 were included, in English and Portuguese, with free access to the full text. The inclusion criteria included systematic reviews and meta -analyses that addressed the relationship between lifestyle, lipid metabolism and cell damage. Duplicate studies were excluded, as well as those that were not directly related to the investigated theme. Initially, 10 studies were identified, of which 8 met the eligibility criteria and were selected for t he final analysis. The results show that dietary patterns rich in sodium, sugars, saturated fats and chemical additives, combined with physical inactivity, favor excessive lipid synthesis, reduce the use of lipids as an energy source and facilitate lipotox icity. This metabolic scenario increases mitochondrial overload, increases the generation of reactive oxygen species, induces inflammatory pathways and mitochondrial -mediated cellular apoptosis. Therefore, lipotoxicity emerges as a central pathophysiologic al liong between bad lifestyle habits and cellular changes that are correlated to the onset of chronic diseases. However, the methodological diversity in the studies makes it difficult to standardize the findings. The findings reinforce that ultra-processed foods and sedentary behavior act as central metabolic determinants of lipotoxicity and cell damage, highlighting the need for an integrated approach to prevent such effects by promoting healthy eating patterns and physical activity to minimize metabolic risks.