| Texto completo | |
| Autor(es): |
Schmitt, Luisa O.
;
Blanco, Antonella
;
Lima, Sheila V.
;
Mancini, Gianni
;
Mendes, Natalia F.
;
Latini, Alexandra
;
Gaspar, Joana M.
Número total de Autores: 7
|
| Tipo de documento: | Artigo Científico |
| Fonte: | METABOLITES; v. 14, n. 3, p. 18-pg., 2024-03-01. |
| Resumo | |
Consumption of high-fat diets (HFD) is associated with brain alterations, including changes in feeding behavior, cognitive decline, and dementia. Astrocytes play a role in HFD-induced neuroinflammation and brain dysfunction; however, this process is not entirely understood. We hypothesized that exposure to saturated fatty acids can compromise astrocyte viability and mitochondrial function. The C6 (astrocytes) cell line was treated with palmitate or stearate (200 mu M and 400 mu M) for 6 h. Cell viability, morphology, inflammatory markers, and oxidative stress were evaluated. To assess mitochondrial function, various parameters were measured (membrane potential, mass, respiration, and complex activities). We observed that 6 h of treatment with 400 mu M palmitate decreased cell viability, and treatment with 200 mu M palmitate changed the astrocyte morphology. Palmitate increased inflammatory markers (TNF-alpha and IL6) but did not induce oxidative stress. Palmitate significantly decreased the mitochondrial membrane potential and mitochondrial mass. Complex I activity also decreased in palmitate-treated cells; however, no changes were observed in mitochondrial respiration. In conclusion, palmitate, a saturated fatty acid, induces inflammation and impairs mitochondrial function, leading to reduced astrocytic cell viability and changes in cellular morphology. Our study provides valuable insights into the potential mechanisms underlying the relationship between saturated fatty acids, astrocytes, and mitochondrial function in obesity-related brain dysfunction. (AU) | |
| Processo FAPESP: | 22/06282-7 - Envolvimento da via CXCL12/CXCR4 na quimiotaxia de monócitos e na neurogênese pós-natal durante a inflamação hipotalâmica e da obesidade materna no dimorfismo sexual de monócitos |
| Beneficiário: | Natália Ferreira Mendes |
| Modalidade de apoio: | Auxílio à Pesquisa - Projeto Geração |
| Processo FAPESP: | 23/07393-0 - Envolvimento da via CXCL12/CXCR4 na quimiotaxia de monócitos e na neurogênese pós-natal durante a inflamação hipotalâmica e da obesidade materna no dimorfismo sexual de monócitos |
| Beneficiário: | Natália Ferreira Mendes |
| Modalidade de apoio: | Bolsas no Brasil - Projeto Geração |