Approximately 100 years ago, the cholesterol-lowering effects of soy protein compared with animal protein were reported in rabbits (Ignatowsky, 1908). Since then, many studies have reported the effects of soy proteins on serum lipids in humans; however, results have been inconsistent, possibly because of different experimental conditions, such as soy protein content in the diet and degree of hypercholesterolemia in the subjects. In a meta-analysis published in 1995, Anderson et al. concluded that soy protein consumption significantly decreased serum levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and TG, corresponding to the degree of hypercholesterolemia. Based on these findings, the U.S. Food and Drug Administration granted the following health claim for soy protein in 1999: "25 grams of soy protein a day, as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease."
Most commercially available SPI products contain significant amounts of genistein, daidzein, and glycitein. These isoflavones have been shown to exert strong biological actions in animals, such as serum cholesterol lowering, arterial vasodilation, and atherosclerosis inhibition (Sacks et al, 2006). Hence, these isoflavones were assumed to be largely responsible for the beneficial effects of SPI on hypercholesterolemia in humans. Human studies comparing the effects of casein, animal proteins, and ethanol-washed isoflavone-free SPI on serum cholesterol levels have demonstrated declines in LDL cholesterol with isoflavone-free soy protein consumption (Jenkins et al, 2002; Lichtenstein et al, 2002). Furthermore, studies comparing the effects of SPI with or without isoflavones confirmed that isoflavones are not responsible for the lipid-lowering effects in humans. However, the soy protein component(s) responsible for this effect is not known. Candidates include a peptide derived from glycinin that inhibits reabsorption of bile acid from the intestine (Nagaoka et al, 1997) and LPs that have been shown to reduce serum cholesterol (Kanamoto et al, 2007). However, these studies were performed in rats; the effects of glycinin and soy LPs in humans are unclear. Thus, identification of components responsible for cholesterol lowering remains unsolved.
The effects of LP-free b-conglycinin were assessed by supplementation of the diets of adults with high plasma TG. Intake of b-conglycinin (5 g/day) normalized serum TG and reduced visceral fat in subjects with body mass indices between 25 and 30 (Kohno et al, 2006). Based on these findings, in 2007, soy b-conglycinin was approved as a food for specified health use in Japan.
The plasma TG level is controlled by the amount of very low-density lipoprotein (VLDL) secreted from the liver and the rate of VLDL-TG catabolism in blood. To determine the effects of soy b-conglycinin on lipid metabolism, small peptides were derived from LP- and isofla-vone-free b-conglycinin by protease digestion and used to treat the human hepatocellular carcinoma cell line HepG2 (Mochizuki et al, 2009). The findings showed that the b-conglycinin-derived peptides suppressed TG synthesis, thereby suppressing the secretion of VLDL from HepG2 cells into the medium.
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