This study compared the contents of ginsenosides depending on steaming conditions of red ginsengs to provide basic information for developing functional foods using red ginsengs. The red ginseng steamed eight times at 98℃ ranked atop the amounts of prosapogenins ever detected in red ginsengs (ginsenoside Rg2, Rg3, Rg5, Rg6, Rh1, Rh4, Rk1, Rk3, F1, F4, 1.15%) among red ginsengs steamed more than twice. When steamed eight times at 98℃, 2.7 times as much prosapogenins such as ginsenosides Rg2, Rg3, Rg5, Rg6, Rh1, Rh4, Rk1, Rk3, F1, and F4 as those steamed just once at 98℃ was collected. In addition, the red ginsengs steamed eight times at 98℃ contained more amounting ginsenoside Rg3 (0.28%) than that in the red ginseng steamed several times at random. Accordingly, it is recommendable that red ginsengs steamed 8 times, which proved to be the optimal steaming condition, be used rather than those steamed 9 times (black ginsengs), in order to develop red ginseng products of high prosapogenin concentration and high functions.
Beneficial effect of eugenol on fatty liver was examined in hepatocytes and liver tissue of high fat diet (HFD)-fed C57BL/6J mice. To induce a fatty liver, palmitic acid or isolated hepatocytes from HFD-fed Sprague-Dawley (SD) rats were used in vitro studies, and C57BL/6J mice were fed HFD for 10 weeks. Lipid contents were markedly decreased when hepatocytes were treated with eugenol for up to 24 h. Gene expressions of sterol regulatory element binding protein 1 (SREBP1) and its target enzymes were suppressed but those of lipolysis-related proteins were increased. As a regulatory kinase for lipogenic transcriptional factors, the AMP-activated protein kinase (AMPK) signaling pathway was examined. Protein expressions of phosphorylated Ca 2 -calmodulin dependent protein kinase kinase (CAMKK), AMPK and acetyl-CoA carboxylase (ACC) were significantly increased and those of phosphorylated mammalian target of rapamycin (mTOR) and p70S6K were suppressed when the hepatocytes were treated with eugenol at up to 100 µM. These effects were all reversed in the presence of specific inhibitors of CAMKK, AMPK or mTOR. In vivo studies, hepatic triglyceride (TG) levels and steatosis score were decreased by 45% and 72%, respectively, in eugenoltreated mice. Gene expressions of fibrosis marker protein such as α-smooth muscle actin (α-SMA), collagen type I (Col-I) and plasminogen activator inhibitor-1 (PAI-1) were also significantly reduced by 36%, 63% and 40% in eugenol-treated mice. In summary, eugenol may represent a potential intervention in populations at high risk for fatty liver.Key words eugenol; fatty liver; fibrosis; AMP-activated protein kinase; sterol regulatory element binding protein Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver ailment worldwide.1) While hepatic steatosis is often asymptomatic, it can progress to non-alcoholic steatohepatitis (NASH). If untreated, NASH can progress to cirrhosis and increased risk of early mortality.2) Obesity and insulin resistance, as seen in type 2 diabetes mellitus (T2DM), and hypertriglyceridemia are well-documented risk factors for NAFLD.3) These factors are key targets for prevention and therapy of NAFLD tends to focus on addressing the obesity or insulin resistance rather than NAFLD itself. NAFLD in the hepatic steatosis (HS) phase can be reversed by lifestyle modification, while NASH is more difficult to treat. Thus, preventing the progression of HS to NASH is of primary importance. Lifestyle recommendations for NAFLD are generally limited to losing weight through energy restriction and/or increasing physical activity, which is often to fail to hold on to them. With this notion, phytochemicals obtained from medicinal plants or foods are attracting alternative options for the treatment of NAFLD and prevention to progress to NASH.
BACKGROUND/OBJECTIVESIncreased consumption of instant noodles has recently been reported to be positively associated with obesity and cardiometabolic syndrome in South Korea, which has the highest per capita instant noodle consumption worldwide. This study aimed to investigate the association between instant noodle consumption and cardiometabolic risk factors among college students in Seoul.SUBJECTS/METHODSThe study subjects consisted of 3,397 college students (1,782 male; 1,615 female) aged 18-29 years who participated in a health checkup. Information on instant noodle consumption was obtained from the participants' answers to a question about their average frequency of instant noodle intake over the 1 year period prior to the survey.RESULTSStatistical analysis using a general linear model that adjusted for age, body mass index, gender, family income, health-related behaviors, and other dietary factors important for cardiometabolic risk, showed a positive association between the frequency of instant noodle consumption and plasma triglyceride levels, diastolic blood pressure, and fasting blood glucose levels in all subjects. Compared to the group with the lowest frequency of instant noodle intake (≤ 1/month), the odds ratio for hypertriglyceridemia in the group with an intake of ≥ 3/week was 2.639 [95% confidence interval (CI), 1.393–5.000] for all subjects, while it was 2.149 (95% CI, 1.045–4.419) and 5.992 (95% CI, 1.859–21.824) for male and female students, respectively. In female students, diastolic blood pressure was also higher among more frequent consumers of instant noodles.CONCLUSIONSOur results suggest that frequent consumption of instant noodles may be associated with increased cardiometabolic risk factors among apparently healthy college students aged 18–29 years.
The inhibitory effect of betulinic acid (BA) on hepatic glucose production was examined in HepG2 cells and high fat diet (HFD)-fed ICR mice. BA significantly inhibited the hepatic glucose production (HGP) and gene expression levels of PGC-1α, PEPCK, and G6Pase. BA activated AMPK and suppressed the expression level of phosphorylated CREB. These effects were all abolished in the presence of compound C (an AMPK inhibitor). Moreover, inhibition of AMPK by overexpression of dominant negative AMPK prevented BA from suppression of HGP, indicating that the inhibitory effect of BA on HGP is AMPK-dependent. In addition, BA markedly phosphorylated CAMKK, and phosphorylation of AMPK and ACC, and suppression of HGP were all reversed in the presence of STO-609 (a CAMKK inhibitor), suggesting that CAMKK is an upstream kinase for AMPK. In an animal study, HFD-fed ICR mice were orally administered with 5 or 10 mg of BA per kg (B5 and B10) for three weeks. Plasma glucose, triglyceride, and the insulin resistance index of the B10 group were decreased by 34%, 59%, and 38%, respectively. In a pyruvate tolerance test, pyruvate-induced glucose excursion was decreased by 27% when mice were pretreated with 10 mg/kg of BA. In summary, BA effectively ameliorates hyperglycemia through inhibition of hepatic gluconeogenesis via modulating the CAMKK-AMPK-CREB signaling pathway.
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