Jump to Main Content
Induction of Cd36 expression elicited by fish oil PUFA in spontaneously hypertensive rats
- Alexander Aguilera, A., Hernandez Diaz, G., Lara Barcelata, M., Angulo Guerrero, O., Oliart Ros, R.M.
- Journal of nutritional biochemistry 2006 v.17 no.11 pp. 760-765
- rats, animal disease models, portal hypertension, metabolic syndrome, etiology, chromosome elimination, fish oils, omega-3 fatty acids, polyunsaturated fatty acids, dietary fat, fat intake, nutrition-genotype interaction, free fatty acids, peroxisomes, messenger RNA, blood lipids, low density lipoprotein, high density lipoprotein, insulin, triacylglycerols
- Cd36 is an integral membrane glycoprotein expressed on the surface of cells active in fatty acid metabolism (adipocytes, muscle cells, platelets, monocytes, heart and intestine cells). This protein plays diverse functions including uptake of long-chain fatty acids and oxidized low-density lipoproteins. A recent report demonstrates that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridemia in spontaneously hypertensive rats (SHRs). Cd36 is a tightly regulated protein whose expression is modulated through peroxisome proliferator-activated receptor (PPAR) transcription factors, by conditions that alter lipid metabolism such as diabetes mellitus and high-fat feeding. The purpose of this study was to evaluate the effect of dietary fish oil, rich in n-3 polyunsaturated fatty acids (PUFAs), on metabolic parameters and on the expression levels of Cd36 in adipose tissue in the SHR. Spontaneously hypertensive rats showed lower Cd36 mRNA levels when compared to Kyoto-Wistar (KW) rats (control). After 6 weeks of fish oil (FO) administration, this group of SHRs (FO-SHR) presented increased levels of Cd36 mRNA, concomitantly with decreased insulin, free fatty acids (FFAs), triglycerides, cholesterol, LDL, HDL, total lipids and blood pressure, in comparison to control rats that received a corn-canola oil diet. The study confirmed the beneficial effects of fish oil administration on the metabolic syndrome, suggesting that the induction of Cd36 expression could be one of the molecular mechanisms elicited by fish oil PUFAs.