NUCLEAR RECEPTORS, HEPATIC LIPID DROPLETS IN SUCROSE INDUCED LIPIDOGENESIS: REVERTION BY N-3 PUFA

BRENNER, RR; BERNASCONI, AM; HEIN, GJ; MONTANARO, MA; PELLON-MAISON M; CHICCO, A; LOMBARDO, YB

San Miguel de Tucumán

Congreso; XLV Reunión Anual de la Sociedad Argentina de Investigación Bioquímica (SAIB); 2009

SAIB

The sucrose rich diet (SRD) that mimicks non insulin dependent diabetes revealed dependence of liver triacylglycerols (TG) and cholesterol esters (CE) levels with lipidogenic LXR antilipidogenic PPAR-a and dietary polyunsaturated fatty acids (PUFA) of n-3 series. Plasmatic and hepatic increases of TG and NEFA were produced after SRD feeding with normal insulinemia correlated to decreases of PPAR-a and its RE dependent enzymes and increases of lipogenic LXR-a and FA synthase (FS) whereas the stearoyl-CoA desaturase-1 was depressed. Hepatic TG and CE were mainly compartmentalized in lipid droplets. Administration of cod liver oil (7%) reverted the abnormal increases normalizing PPAR-a and its RE dependent enzymes as well as depressing LXR-a and FS and glucose-6-phosphate dehydrogenase. In liver lipids 20:4n-6 was depressed whereas n-3 PUFA were enhanced without variation of 18:1 n-9/18:0 ratio. In hepatic lipid droplets of SRD fed rats the high levels (33%) of 16:0 and 18:1 n-9 of TG were unmodified while 18:2 n-6 was depressed to half (9%) and low 20:4 n-6 was replaced by similar proportion of n-3 PUFAs. In CE the low 20:4 n-6 was little decreased and n-3 PUFA appear. Therefore hepatic lipidogenesis is mainly regulated by PPAR-a and LXR-a, and neutral lipids of lipid droplets behave rather as selective dynamic reservoir of monoenoic and saturated FAs but not of PUFA.a and its RE dependent enzymes and increases of lipogenic LXR-a and FA synthase (FS) whereas the stearoyl-CoA desaturase-1 was depressed. Hepatic TG and CE were mainly compartmentalized in lipid droplets. Administration of cod liver oil (7%) reverted the abnormal increases normalizing PPAR-a and its RE dependent enzymes as well as depressing LXR-a and FS and glucose-6-phosphate dehydrogenase. In liver lipids 20:4n-6 was depressed whereas n-3 PUFA were enhanced without variation of 18:1 n-9/18:0 ratio. In hepatic lipid droplets of SRD fed rats the high levels (33%) of 16:0 and 18:1 n-9 of TG were unmodified while 18:2 n-6 was depressed to half (9%) and low 20:4 n-6 was replaced by similar proportion of n-3 PUFAs. In CE the low 20:4 n-6 was little decreased and n-3 PUFA appear. Therefore hepatic lipidogenesis is mainly regulated by PPAR-a and LXR-a, and neutral lipids of lipid droplets behave rather as selective dynamic reservoir of monoenoic and saturated FAs but not of PUFA.a and its RE dependent enzymes as well as depressing LXR-a and FS and glucose-6-phosphate dehydrogenase. In liver lipids 20:4n-6 was depressed whereas n-3 PUFA were enhanced without variation of 18:1 n-9/18:0 ratio. In hepatic lipid droplets of SRD fed rats the high levels (33%) of 16:0 and 18:1 n-9 of TG were unmodified while 18:2 n-6 was depressed to half (9%) and low 20:4 n-6 was replaced by similar proportion of n-3 PUFAs. In CE the low 20:4 n-6 was little decreased and n-3 PUFA appear. Therefore hepatic lipidogenesis is mainly regulated by PPAR-a and LXR-a, and neutral lipids of lipid droplets behave rather as selective dynamic reservoir of monoenoic and saturated FAs but not of PUFA.a and LXR-a, and neutral lipids of lipid droplets behave rather as selective dynamic reservoir of monoenoic and saturated FAs but not of PUFA.