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Exogenous FAs are stored in lipid droplets (LDs) after intake, chelating excess FAs in the form of TAG and sterol esters to avoid cell damage

1000 mg

These results collectively indicate that targeting mitochondrial oxidative stress represents a promising therapeutic approach for mitigating diabetic cardiovascular complications through the preservation of mitochondrial function, attenuation of cellular damage, and reinforcement of cardioprotective mechanisms

B.G.Ng, P.Sosicka, S.Agadi, M.Almannai, C.A.Bacino, R.Barone, L.D.Botto, J.E.Burton, C.Carlston, B.Hon-Yin Chung, J.S.Cohen, D.Coman, K.M.Dipple, N.Dorrani, W.B.Dobyns, A.F.Elias, L.Epstein, W.A.Gahl, D.Garozzo, T.B.Hammer, J.Haven, D.Hron, M.Herzog, G.E.Hoganson, J.M.Hunter, M.Jain, J.Juusola, S.Lakhani, H.Lee, J.Lee, K.Lewis, N.Longo, C.Marques Loureno, C.C.Y.Mak, D.McKnight, B.A.Mendelsohn, C.Mignot, G.Mirzaa, W.Mitchell, H.Muhle, S.F.Nelson, M.Olczak, C.G.S.Palmer, A.Partikian, M.C.Patterson, T.M.Pierson, S.C.Quinonez, B.M.Regan, M.E.Ross, M.J.Guillen Sacoto, F.Scaglia, I.E.Scheffer, D.Segal, N.Shah Singhal, P.Striano, L.Sturiale, J.D.Symonds, S.Tang, E.Vilain, M.Willis, L.A.Wolfe, H.Yang, S.Yano, Z.Powis, S.F.Suchy, J.A.Rosenfeld, A.C.Edmondson, S.Grunewald, H.H.Freeze SLC35A2-CDG: Functional characterization, expanded molecular, clinical, and biochemical phenotypes of 30 unreported Individuals Human Mutation 40(7), 908-925 (2019) DOI: Abstract: Pathogenic de novo variants in the X-linked gene SLC35A2 encoding the major Golgi-localized UDP-galactose transporter required for proper protein and lipid glycosylation cause a rare type of congenital disorder of glycosylation known as SLC35A2-congenital disorders of glycosylation (CDG

Quantification and statistical analysis All grouped data are presented as mean SD or SEM from studies performed at least in triplicate unless otherwise specified