“Effect of dietary Salba seed (Salvia hispanic L) on liver lipogenic-oxidative enzymes and nuclear receptors PPARα and SREBP-1 in a dyslipemic insulin resistance (IR) rat model”.

LOMBARDO Y.B; ROSSI ANDREA; OLIVA M.E.; CHICCO A

Roma

Simposio; • 29th International Symposium on Diabetes and Nutrition of the Nutrition Study Group (DNSG) of the EASD; 2011

Salba, a variety of chia seed rich in 18:3, n-3 ALA, administered as a dietary fat, prevents the onset of dyslipidemia and IR in rats fed for 3 weeks a sucrose-rich diet (SRD). Dyslipidemia, liver esteatosis an IR induced by long-term (5 months) SRD feeding were improved when chia replaced corn oil (CO) in the diet during the last two months of the feeding period. Changes in the fat of lipids (lipogenesis-oxidation) could prevent-improve dyslipidemia. This study analyzed the effect of dietary chia seed in rats fed a SRD for either 3 weeks or 5 months upon: i) hepatic key enzyme activities involved in lipid metabolism: FAS, ACC, G6PDH, CPT-1 and FAO; ii) the protein mass expression of PPAR α and SREBP-1. Methodology: 1-Wistar rats were fed 3 weeks either a SRD (%w/w: 65.9 sucrose, 11 CO, 15 protein) or SRD in which CO was replaced by chia seed (SRD+chía). 2- Rats were fed SRD 3 months. After that, half of the rats continued with the SRD while in the other half CO was replaced by chia for 2 months (SRD+chía). A reference group consumed a control diet all the time. Liver and plasma triglycerides (Tg) and the parameters mentioned in i & ii were analyzed in all groups. Results: The replacement of CO by chia in the SRD prevented (3 weeks) or normalized (5 months) the increase of liver and plasma Tg, FAS, ACC and G6-PDH activities and increased (p<0.05) CPT-1 and FAO activities. Protein mass of PPAR α increased (p<0.05) in both protocols. SREBP-1 protein mass which was increased in the SRD was normalized by chia. Conclussions: The results suggest that dietary chia seed normalized plasma and liver Tg by increasing the protein mass of nuclear receptor PPAR α and fatty acid oxidation and reducing SREBP-1 protein mass and lipogenesis.