A water-soluble extract of chicken reduced plasma triacylglycerols, but showed no anti-atherosclerotic activity in apoE−/− mice

Abstract Background A water-soluble protein extract of chicken (CP) has been reported to modulate plasma lipids and hepatic lipid catabolism. Atherosclerosis is the primary contributing factor of cardiovascular disease and there is evidence that both lipid abnormalities and chronic inflammation have crucial involvement in the initiation and progression of atherosclerosis. The aim of the study was to assess the impact of CP on atherosclerotic development in mice predisposed for developing atherosclerotic lesions. Methods 24 apoE −/− mice were divided into two groups and fed a high-fat diet. The control group received a 20% casein diet, whereas the intervention group was fed a diet with 15% chicken protein and 5% casein. Body weight and feed intake was measured regularly, and indirect calorimetry was measured at week 1 and 10. After 12 weeks the mice were sacrificed, and blood, liver, heart and aorta were harvested. Plasma and liver lipids and fatty acid composition analyses were carried out, in addition to gene expression in liver and heart. Also, en-face analysis was performed on aorta, and plasma inflammatory markers were determined. Results The dietary intervention with CP only resulted in minor reduction of plasma triacylglycerol (TAG) and no change in the plasma cholesterol level compared to control. The TAG lowering was associated with induction of hepatic carnitine acyltransferase 2 activity and gene expression. Mice fed CP also displayed a lower respiratory exchange ratio during the light cycle, indicating a higher degree of fatty acid oxidation in the fasting state. Aorta images displayed no differences in plaque development between mice fed CP or control diet, and gene expression of inflammatory markers in heart was unchanged. Moreover, CP administration did not influence plasma levels of several inflammatory cytokines and chemokines in apoE −/− mice. Conclusion Chicken protein displayed a slight potential to increase mitochondrial fatty acid oxidation and reduce plasma TAG. However, CP did not affect plasma cholesterol levels, inflammation status or atherosclerotic development in apoE −/− mice. Based on these results, dietary intervention with CP does not have sufficient capacity to influence atherosclerotic development in apoE −/− mice.