Abstract
Soy protein and fish oil are food components that decrease the risk of cardiovascular disease. Previous studies demonstrated that these food components reduced serum cholesterol levels and suppressed hepatic lipogenesis. However, the underlying mechanisms of action of these food components remain unclear. Ten classes of serum lipoprotein profiles showed that dietary tofu, a soybean curd, suppressed cholesterol absorption, while fish oil reduced most of the lipoprotein classes in rats. Tofu and fish oil both halved the level of the lipoprotein class LAC1 (LDL-anti-protease complex), a 15-nm LDL-anti-protease complex, which is speculated to be a cause of atherosclerosis. Moreover, a global transcriptome analysis revealed that tofu inhibited the mRNA expression of genes involved in hepatic lipogenesis, while fish oil stimulated that of genes related to fatty acid degradation. Therefore, tofu and fish oil independently regulate lipid metabolism. The decrease observed in LAC1 may have been due to reduced cholesterol absorption in the tofu diet group and the interference of lipogenesis via the activation of polyunsaturated fatty acid detoxification in the fish oil group.
Highlights
Cardiovascular disease, a leading cause of death worldwide, is associated with atheroma
A previous study reported that the high-molecular-weight fraction (HMF), a fraction increased by the coagulation and freeze-drying of tofu protein, may increase fecal weight and has a high bile acid-binding capacity [22]
Changes in the particle sizes of LDL by tofu may reflect differences in apoproteins, which influences the qualitative properties of lipoproteins
Summary
Cardiovascular disease, a leading cause of death worldwide, is associated with atheroma. Its major direct cause appears to be the rupture of atherosclerotic plaques [1], and focal arterial inflammatory activity is one of its most prominent characteristics [2]. Continuous exposure to inflammation or other types of endothelial activation increases vascular permeability, thereby allowing excess lipid infiltration in the intima and promoting transmigration on immune cells and monocytes, resulting in the formation of an atherosclerotic plaque [3]. The formation of fragile and leaky vessels that invade the expanding intima concomitantly contributes to enlarging the necrotic core, which increases the vulnerability of the plaque [3].
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