RT Journal Article
T1 Elovl2-Ablation leads to mitochondrial membrane fatty acidremodeling and reduced efficiency in mouse liver mitochondria
A1 Gómez Rodríguez, Alexia
A1 Talamonti, Emanuela
A1 Naudí, Alba
A1 Kalinovich, Anastasia V.
A1 Pauter, Anna M.
A1 Barja de Quiroga, Gustavo
A1 Bengtsson, Tore
A1 Jacobsson, Anders
A1 Pamplona, Reinald
A1 Shabalina, Irina G.
AB The fatty acid elongase elongation of very long-chain fatty acids protein 2 (ELOVL2) controls the elongation of polyunsaturated fatty acids (PUFA) producing precursors for omega-3, docosahexaenoic acid (DHA), and omega-6, docosapentaenoic acid (DPAn-6) in vivo. Expectedly, Elovl2-ablation drastically reduced the DHA and DPAn-6 in liver mitochondrial membranes. Unexpectedly, however, total PUFAs levels decreased further than could be explained by Elovl2 ablation. The lipid peroxidation process was not involved in PUFAs reduction since malondialdehyde-lysine (MDAL) and other oxidative stress biomarkers were not enhanced. The content of mitochondrial respiratory chain proteins remained unchanged. Still, membrane remodeling was associated with the high voltage-dependent anion channel (VDAC) and adenine nucleotide translocase 2 (ANT2), a possible reflection of the increased demand on phospholipid transport to the mitochondria. Mitochondrial function was impaired despite preserved content of the respiratory chain proteins and the absence of oxidative damage. Oligomycin-insensitive oxygen consumption increased, and coefficients of respiratory control were reduced by 50%. The mitochondria became very sensitive to fatty acid-induced uncoupling and permeabilization, where ANT2 is involved. Mitochondrial volume and number of peroxisomes increased as revealed by transmission electron microscopy. In conclusion, the results imply that endogenous DHA production is vital for the normal function of mouse liver mitochondria and could be relevant not only for mice but also for human metabolism
PB MDPI
SN Electronic: 2072-6643
YR 2022
FD 2022-01-27
LK https://hdl.handle.net/20.500.14352/71806
UL https://hdl.handle.net/20.500.14352/71806
LA eng
NO Ministerio de Ciencia e Innovación y Universidades (MICINN)
NO Generalitat de Cataluña. Agencia de Gestión de Ayudas Universitarias y de Investigación/Fondo Europeo de Desarrollo Regional (FEDER)
NO Swedish Science Council
DS Docta Complutense
RD 19 abr 2025