Abstract
Fish consumption is considered health beneficial as it decreases cardiovascular disease (CVD)-risk through effects on plasma lipids and inflammation. We investigated a salmon protein hydrolysate (SPH) that is hypothesized to influence lipid metabolism and to have anti-atherosclerotic and anti-inflammatory properties. 24 female apolipoprotein (apo) E−/− mice were divided into two groups and fed a high-fat diet with or without 5% (w/w) SPH for 12 weeks. The atherosclerotic plaque area in aortic sinus and arch, plasma lipid profile, fatty acid composition, hepatic enzyme activities and gene expression were determined. A significantly reduced atherosclerotic plaque area in the aortic arch and aortic sinus was found in the 12 apoE−/− mice fed 5% SPH for 12 weeks compared to the 12 casein-fed control mice. Immunohistochemical characterization of atherosclerotic lesions in aortic sinus displayed no differences in plaque composition between mice fed SPH compared to controls. However, reduced mRNA level of Icam1 in the aortic arch was found. The plasma content of arachidonic acid (C20∶4n-6) and oleic acid (C18∶1n-9) were increased and decreased, respectively. SPH-feeding decreased the plasma concentration of IL-1β, IL-6, TNF-α and GM-CSF, whereas plasma cholesterol and triacylglycerols (TAG) were unchanged, accompanied by unchanged mitochondrial fatty acid oxidation and acyl-CoA:cholesterol acyltransferase (ACAT)-activity. These data show that a 5% (w/w) SPH diet reduces atherosclerosis in apoE−/− mice and attenuate risk factors related to atherosclerotic disorders by acting both at vascular and systemic levels, and not directly related to changes in plasma lipids or fatty acids.
Highlights
Cardiovascular disease (CVD) is responsible for approximately 16–17 million deaths annually, making it the leading cause of mortality in Western countries [1,2]
A significantly lower plaque development was observed in the aortic arch in salmon protein hydrolysate (SPH)-fed mice compared to control mice (0.5560.33 vs. 1.6360.996106 mm2; Fig. 1, corresponding to 0.9160.55 vs. 2.7261.72% of the aortic surface covered by plaque)
There were no differences in thoracic (1.0860.47 vs. 0.8560.416106 mm2; Fig. 1, corresponding to 1.7160.84 vs. 1.4160.68% of the aortic surface covered by plaque) or abdominal aorta sections (0.8160.53 vs. 0.7860.536106 mm2; Fig. 1, corresponding to 1.3660.89 vs. 1.2960.88% of the aortic surface covered by plaque)
Summary
Cardiovascular disease (CVD) is responsible for approximately 16–17 million deaths annually, making it the leading cause of mortality in Western countries [1,2]. The disease encompasses conditions such as coronary artery disease, carotid and cerebral atherosclerotic disease and peripheral artery atherosclerosis resulting in chronic and acute ischemia in affected organs. The underlying pathological process is lipid accumulation leading to atherosclerosis, a slowly progressing chronic disorder of large and medium-sized arteries that can lead to intravascular thrombosis with subsequent development of complications like myocardial infarction (MI), stroke and acute ischemia of the limb [3]. Inflammation has emerged as an additional key factor in the development of atherosclerosis and seems to be involved in all stages, from the small inflammatory infiltrate in the early lesions, to the inflammatory phenotype characterizing an unstable and rupture-prone atherosclerotic lesion [4]. Inflammation in atherosclerosis leads to activation of endothelial cells, enhanced expression of adhesion molecules, inflammatory cytokines and macrophage accumulation
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