Liver mitochondrial membrane fluidity at early development of diabetes and its correlation with the respiration.
The biological membranes are important in cell function but, during development of diseases such as diabetes, they are impaired. Consequently, membrane-associated biological processes are impaired as well. The mitochondria are important organelles where oxidative phosphorylation takes place, a process closely related with the membranes. In general, it is accepted that the development process of diabetes decreases membrane fluidity. However, in some cases, it has been found to increase membrane fluidity of mitochondria but to decrease the Respiratory Control (RC) index. In this study we found an increase of membrane fluidity and an increase of the RC at an early phase of the development of a type 2 diabetes model. We measured the lipoperoxidation, analyzed the fatty acids composition by gas chromatography, and assessed membrane fluidity using three fluorescent monitors located at different depths inside the bilayer, dipyrenilpropane (DPyP), diphenylhexatriene (DPH), and trimethylammonium diphenylhexatriene (TMA-DPH). Our findings indicate that in the initial stage of diabetes development, when lipoperoxidation still is not significant, the membrane fluidity of liver mitochondria increases because of the increment in the unsaturated to saturated fatty acids ratio (U/S), thus producing an increase of the RC. The membrane fluidity is not the same at all depths in the bilayer. Contrary to the results obtained in mitochondria, the diabetes induced a decrease in the U/S fatty acids ratio of liver total lipids, indicating that the mitochondria might have an independent mechanism for regulating its fatty acids composition.
Unidad de Biomedicina, FES Iztacala, UNAM, Av. De los Barrios No. 1, Los Reyes Iztacala, 54090, Tlalnepantla, Estado de México, C.P., Mexico.
Ismael H
IH
Pérez-Hernández
Unidad de Biomedicina, FES Iztacala, UNAM, Av. De los Barrios No. 1, Los Reyes Iztacala, 54090, Tlalnepantla, Estado de México, C.P., Mexico.
Josué Misael
JM
Domínguez-Fuentes
Unidad de Morfofisiología, FES Iztacala, UNAM, Av. De los Barrios No. 1, Los Reyes Iztacala, 54090, Tlalnepantla, Estado de México, C.P., Mexico.
Martín
M
Palomar-Morales
Depto. Biomedicina Cardiovascular, Instituto Nacional de Cardiología I.Ch, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, 14080, Ciudad de México, Mexico.
Ana Cecilia
AC
Zazueta-Mendizabal
Unidad de Morfofisiología, FES Iztacala, UNAM, Av. De los Barrios No. 1, Los Reyes Iztacala, 54090, Tlalnepantla, Estado de México, C.P., Mexico.
Arturo
A
Baiza-Gutman
Unidad de Biomedicina, FES Iztacala, UNAM, Av. De los Barrios No. 1, Los Reyes Iztacala, 54090, Tlalnepantla, Estado de México, C.P., Mexico. rmejia@unam.mx.
Ricardo
R
Mejía-Zepeda
D000818:Animals; D019069:Cell Respiration; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology*; D005227:Fatty Acids / Q000032:analysis; D008054:Lipid Peroxides / Q000032:analysis; D008560:Membrane Fluidity; D008930:Mitochondria, Liver / Q000737:chemistry / Q000648:ultrastructure*; D051336:Mitochondrial Membranes; D010085:Oxidative Phosphorylation; D017208:Rats, Wistar
D005227:Fatty Acids; D008054:Lipid Peroxides
Diabetes; Fatty acids composition; Liver; Membrane fluidity; Mitochondria; Respiratory control