Fish protein increases circulating levels of trimethylamine‐ N‐oxide and accelerates aortic lesion formation in apoE null mice

• Published in: Molecular Nutrition & Food Research
• Main Authors: Yazdekhasti, Narges, Brandsch, Corinna, Schmidt, Nadine, Schloesser, Anke, Huebbe, Patricia, Rimbach, Gerald, Stangl, Gabriele I.
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2015
• Subjects: Turbot
• Online Access: http://dx.doi.org/10.1002/mnfr.201500537; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1002%2Fmnfr.201500537; https://onlinelibrary.wiley.com/doi/pdf/10.1002/mnfr.201500537

Scope The protective effect of fish consumption on the cardiovascular system has primarily been ascribed to n‐3 fatty acids, but data investigating the vascular effects of fish protein consumption are scarce. This study aimed to investigate the vascular impact of fish protein in a mouse model of atherosclerosis. Methods and results Male apoE null mice were fed a Western diet containing 20% fish (turbot) protein, casein, or soy protein, for 16 wk. Morphometric analysis of the aorta revealed that the atherosclerotic plaque area of fish protein fed mice was twofold larger than that in casein‐ or soy protein‐fed mice. The percentage area of calcification deposits in plaques of fish protein fed mice was higher (7.57%) than that in casein‐fed (2.86%) or soy protein‐fed (3.46%) mice, and fish protein fed mice exhibited higher plaque expression of CD68, CD36, and IL‐6 than the other two groups. Fish protein intake was accompanied by increased serum concentrations of trimethylamine‐ N ‐oxide (7.03 ± 2.83 μmol/L), as compared with casein (0.92 ± 0.46 μmol/L) and soy protein (1.32 ± 0.54 μmol/L) intake. Conclusion The present data indicate adverse effects of fish protein on the vascular system, which could be attributable to the high serum trimethylamine‐ N ‐oxide concentrations in these mice.