Paweł M. Pisulewski

Functional effects of eggs, naturally enriched with conjugated linoleic acid, on the blood lipid profile, development of atherosclerosis and composition of atherosclerotic plaque in apolipoprotein E and low-density lipoprotein receptor double-knockout mice (apoE/LDLR-/-).

The objective of this study was to evaluate potential anti-atherogenic properties of hen eggs enriched naturally with conjugated linoleic acid (CLA) isomers (cis-9, trans-11 and trans-10, cis-12). Eighteen apoE and LDL receptor double-knockout mice (apoE/LDLR- / - ), at the age of 4 months with pre-established atherosclerosis, were randomly assigned to three experimental groups (n 6) and fed AIN-93G-based diets for the next 2 months. The experimental diets were: AIN-93G+ CLA-free egg-yolk powder (control); AIN-93G+ CLA-free egg-yolk powder +0.1 % CLA (CLA-supplemented eggs); and AIN-93G+ CLA-enriched egg-yolk powder, providing 0.1 % CLA (CLA-enriched eggs). For assessment of anti-atherogenic properties of CLA-enriched or CLA-supplemented eggs the following criteria were used: (1) serum lipid profile; (2) development of atherosclerosis; and (3) composition of atherosclerotic plaque. CLA-enriched eggs, compared with CLA-supplemented eggs, reduced significantly (P < 0.05) total plasma cholesterol in the mice. At the same time, both CLA-supplemented eggs and CLA-enriched eggs tended to decrease the size of atherosclerotic plaque in aortic roots of mice. Most importantly, atherosclerotic plaques of mice fed CLA-enriched eggs showed significantly (P < 0.05) reduced number of atherogenic macrophages and increased area occupied by smooth muscle cells in atherosclerotic lesions. In conclusion, CLA-enriched eggs exerted an anti-inflammatory effect more effectively than CLA-supplemented eggs. This anti-inflammatory effect can be considered their major functional claim that warrants further exploitation.

Effect of conjugated linoleic acid (CLA) on lipid profile and liver histology in laboratory rats fed high-fructose diet

The objective of the study was to assess the effect of CLA on serum lipid profile, plasma malondialdehyde and liver histology in Wistar rats fed high-fructose diet. Eighteen rats were randomly assigned to three experimental groups and fed for the next 21 days. The experimental diets were: I, Control; II, Fructose (63.2% of fructose); and III, CLA+Fructose (1% CLA and 63.2% of fructose). The experimental treatments had no effect on body weight of the rats. The LDL+VLDL cholesterol, TG and liver weight were significantly increased in animals fed Fructose. MDA concentrations were significantly increased in rats fed Fructose diet but CLA+Fructose diet had no effect on this marker. In the same line, the histological examination of the livers showed a series of morphological alterations, notably hepatic steatosis in animals fed high-fructose diet. No signs of the steatosis in rats fed CLA+Fructose diet were observed. In conclusion, CLA in high-fructose diet, decreases serum LDL+VLDL and TG and plasma MDA concentrations as well as liver weight and liver cholesterol, thus opposing the effects of high-fructose diet and showing a potential antiatherogenic effect. Similarly, dietary CLA fed at 1% level (w/w) in high-fructose diet, prevented steatosis observed histologically in livers of rats fed high-fructose diets.