Sweet potato (Ipomoea batatas L.) leaves are consumed as vegetables around the world, especially in Southeast Asia. The aim of this study was to investigate the inhibitory effect of sweet potato leaves on low-density lipoprotein oxidation in vitro and in human subjects. We compared the antioxidant activity of 8 kinds of sweet potato leaves. Every sweet potato leaf had high radical scavenging activity and prolonged a lag time for starting low-density lipoprotein oxidation in vitro. We found that sweet potato leaves contained abundant polyphenol compounds and the radical scavenging activity and prolongation rate of lag time were highly correlated with total polyphenol content. We also confirmed that thiobarbituric acid reactive substances production was increased in endothelial cell-mediated low-density lipoprotein oxidation, which was decreased by treatment with sweet potato leaves. We further measured the low-density lipoprotein oxidizability in 13 healthy volunteers after their intake of 18 g of “Suioh”, raw sweet potato leaves. “Suioh” prolonged a lag time for starting low-density lipoprotein oxidation and decreased low-density lipoprotein mobility. These results suggest that sweet potato leaves have antioxidant activity leading to the suppression of low-density lipoprotein oxidation.

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Enterolactone (ENL) is formed by the conversion of dietary precursors like strawberry lignans via the gut microbiota. Urinary concentrations of lignan metabolites are reported to be significantly associated with a lower risk of Type 2 diabetes (T2D). In the present study, antidiabetic effect of ENL and its modes of action were studied in vitro and in vivo employing a rat skeletal muscle-derived cell line, L6 myocytes in culture, and T2D model db/db mice. ENL dose-dependently increased glucose uptake in L6 myotubes under insulin absent condition. This increase by ENL was canceled by compound C, an inhibitor of 5'-adenosine monophosphate-activated protein kinase (APMK). Activation (=phosphorylation) of AMPK and translocation of glucose transporter 4 (GLUT4) to plasma membrane in L6 myotubes were demonstrated by Western blotting analyses. Promotion by ENL of GLUT4 translocation to plasma membrane was also visually demonstrated by immunocytochemistry in L6 myoblasts that were transfected with glut4 cDNA-coding vector. T2D model db/db mice were fed the basal 20 % casein diet (20C) or 20C supplemented with ENL (0.001 or 0.01 %) for 6 weeks. Fasting blood glucose (FBG) levels were measured every week and intraperitoneal glucose tolerance test (IPGTT) was conducted. ENL at a higher dose (0.01 % in 20C) suppressed the increases in FBG levels. ENL was also demonstrated to improve the index of insulin resistance (HOMA-IR) and glucose intolerance by IPGTT in db/db mice. From these results, ENL is suggested to be an antidiabetic chemical entity converted from dietary lignans by gut microbiota.

Summary Oxidized low-density lipoprotein (LDL) is believed to contribute to atherosclerosis in part by being taken up into macrophages via scavenger receptors, thus accounting for foam cells. Balsamic vinegar is made from grapes and generally consumed in the Mediterranean region. In this study, we investigated the preventive effects of balsamic vinegar on LDL oxidation and foam cell formation. Balsamic vinegar had stronger 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging abilities and higher polyphenol concentrations than rice vinegar. Balsamic vinegar dramatically inhibited LDL oxidation by azoradicals and endothelial cell-mediated oxidation in vitro. Further, we assessed the anti-oxidative effect against LDL after balsamic vinegar consumption in human subjects. Balsamic vinegar prolonged the LDL oxidation lag time and decreased lipid peroxide (LPO) and lyso-phosphatidylcholine (LPC) in LDL particles. We next examined the effect of balsamic vinegar on foam cell formation. Oil red O staining showed that balsamic vinegar inhibited oxidized LDL-induced foam cell formation in THP-1 macrophages. The concentrations of intracellular triglycerides and total cholesterols were reduced in the presence of balsamic vinegar. In addition, balsamic vinegar decreased the mRNA and protein expression level of scavenger receptors in THP-1 macrophages. These results showed that balsamic vinegar contained abundant polyphenols and inhibited LDL oxidation and oxidized LDL-induced foam cell formation by decreasing the expression of scavenger receptors.

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