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Palmitate Compromises C6 Astrocytic Cell Viability and Mitochondrial Function

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Author(s):
Schmitt, Luisa O. ; Blanco, Antonella ; Lima, Sheila V. ; Mancini, Gianni ; Mendes, Natalia F. ; Latini, Alexandra ; Gaspar, Joana M.
Total Authors: 7
Document type: Journal article
Source: METABOLITES; v. 14, n. 3, p. 18-pg., 2024-03-01.
Abstract

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)

FAPESP's process: 22/06282-7 - Involvement of CXCL12/CXCR4 pathway in monocyte chemotaxis and postnatal neurogenesis during hypothalamic inflammation and of maternal obesity in monocyte sexual dimorphism.
Grantee:Natália Ferreira Mendes
Support Opportunities: Generation Project Research Grant
FAPESP's process: 23/07393-0 - Involvement of CXCL12/CXCR4 pathway in monocyte chemotaxis and postnatal neurogenesis during hypothalamic inflammation and of maternal obesity in monocyte sexual dimorphism
Grantee:Natália Ferreira Mendes
Support Opportunities: Scholarships in Brazil - Generation Project