NUCLEAR RECEPTORS AND LIPOGENIC ENZYME RESPONSE TO A DYSLIPEMIC SUCROSE RICH DIET AND ITS REVERTION BY N-3 POLYUNSATURATED FATTY ACIDS

YOLANDA B. LOMBARDO; GUTAVO J. HEIN; ANA BERNASCONI; MAURO MONTANARO; MAGALÍ PELLON-MAISON; GABRIELA FINARELLI; ADRIANA CHICCO; RODOLFO R. BRENNER

Potsdam - Alemania

Simposio; 27th International Symposium on Diabetes and Nutrition; 2009

Diabetes and Nutrition Study Group (DNSG) of the European Association for the Study of Diabetes (EASD)

Objetive: A sucrose rich diet (SRD) induces dyslipidemia and insulin resistance. This study examined: i) The effect of long term feeding a SRD (8 months), on peroxisome-proliferator activated recptor-alpha (PPAR-alpha), liver X receptor-alpha (LXR-alpha), delta-9, delta-6 and delta-5 desaturases mRNA and activities, hepatic enzymes involved in lipid metabolism and fatty acid composition, ii) Possible mechanisms involved the effects n-3 PUFAs, fish oil (FO) on the reversion of dislipidemia. Methodology: Wistar rats were divided into 2 groups. The experimental was fed a SRD (%w/w: 62.5 sucrose, 17 protein, 8 corn oil (CO)). In the control (CD) sucrose was replaced by starch. After 6 months half of the SRD fed rats continued with the SRD, while in the other half (SRD+FO) CO was replaced by FO (%w/w: 7 FO + 1 CO) for 2 months. Beside, half of the rats of the CD continued with the CD, and in the other half CO was replaced by FO (CD+FO) for 2 months. In all groups the parameters mentioned above were measured. Results: SRD increases liver lipogenic enzyme activities without changes in pro-oxidative enzymes. This correlate to a decrease of PPAR-alpha and increase LXR-alpha. SRD depressed delta-9 without altering oleic acid proportion and increasing delta-6 and delta-5 desatruases and 20:4 n-6 fatty acids. The administration of FO depressed LXR-alpha, enhancing PPAR-alpha in control and SRD fed rats and reversed the dyslipidemia. FO increased n-3 and depressed n-6 PUFA of liver lipid not altering the 18:1/18:0 ratio. Conclusions: The results suggest: 1) The contribution of both PPAR-alpha and LXR-alpha interact with the enzymatic effects. 2) The data do not support that hypertriglyceridemia in the SRD is produced by the increase of delta-9 desaturase dependent oleic acid biosynthesis. 3) The effects of FO are mainly produced by competition of dietary n-6 and n-3 FA and not throuth desaturase activity modification.