BackgroundSoy protein and soy peptides have attracted considerable attention because of their potentially beneficial biological properties, including antihypertensive, anticarcinogenic, and hypolipidemic effects. Although soy protein isolate contains several bioactive peptides that have distinct physiological activities in lipid metabolism, it is not clear which peptide sequences are responsible for the triglyceride (TG)-lowering effects. In the present study, we investigated the effects of soy protein-derived peptides on lipid metabolism, especially TG metabolism, in HepG2 cells and obese Otsuka Long-Evans Tokushima fatty (OLETF) rats.ResultsIn the first experiment, we found that soy crude peptide (SCP)-LD3, which was prepared by hydrolyze of soy protein isolate with endo-type protease, showed hypolipidemic effects in HepG2 cells and OLETF rats. In the second experiment, we found that hydrophilic fraction, separated from SCP-LD3 with hydrophobic synthetic absorbent, revealed lipid-lowering effects in HepG2 cells and OLETF rats. In the third experiment, we found that Fraction-C (Frc-C) peptides, fractionated from hydrophilic peptides by gel permeation chromatography-high performance liquid chromatography, significantly reduced TG synthesis and apolipoprotein B (apoB) secretion in HepG2 cells. In the fourth experiment, we found that the fraction with 0.1% trifluoroacetic acid, isolated from Frc-C peptides by octadecylsilyl column chromatography, showed hypolipidemic effects in HepG2 cells. In the final experiment, we found that 3 di-peptides, Lys-Ala, Val-Lys, and Ser-Tyr, reduced TG synthesis, and Ser-Tyr additionally reduced apoB secretion in HepG2 cells.ConclusionNovel active peptides with TG-lowering effects from soy protein have been isolated.
Recent reports have shown that citrus auraptene (7-geranyloxycoumarin) possesses valuable pharmacological properties, including anticarcinogenic, anti-inflammatory, antihelicobacter, antigenotoxic, and neuroprotective effects. In the present study, we investigated the effect of dietary auraptene on hepatic lipid metabolism both in vitro and in vivo. Results suggested that auraptene has the ability to normalize lipid abnormalities in HepG2 hepatocytes. After 4 weeks of auraptene feeding, abdominal white adipose tissue weight and hepatic triglyceride (TG) levels were dose-dependently lowered in Otsuka Long-Evans Tokushima fatty (OLETF) rats. The activities of carnitine palmitoyltransferase, a key enzyme in mitochondrial fatty acid β-oxidation, and peroxisomal β-oxidation were markedly and dose-dependently enhanced in OLETF rat livers by auraptene feeding. Additionally, hepatic expression of acyl-CoA oxidase, the initial enzyme of the peroxisomal β-oxidation system, was significantly and dose-dependently enhanced by auraptene administration. These results suggest that auraptene administration alleviates obesity and hepatic TG accumulation in part through lipolysis enhancement in the livers of obese OLETF rats.
The effect of linoleic acid-menthyl ester (LAME) on lipid metabolism were assessed in HepG2 cells. It is well known that high level of apolipoprotein (apo) B100 in the serum is risk for atherosclerosis. Although linoleic acid (LA) treatment and LA plus L-mentol treatment increased apo B100 secretion, LAME treatment significantly decreased apo B100 secretion in HepG2 cells compared with control medium. The hypolipidemic effect of LAME was attributable to the suppression of triglyceride synthesis in HepG2 cells. It is also known that the risk of coronary heart disease is negatively related to the concentration of serum apo A-1. In the present study, LAME treatment increased apo A-1 secretion as compared with LA treatment in HepG2 cells. These results suggest that mentyl-esterification of fatty acids may be beneficial in anti-atherogenic dietary therapy.
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