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Background: With the increased incidence of diabetes mellitus, the importance of early intervention in prediabetes has been emphasized. We previously reported that fermented kimchi, a traditional Korean food, reduced body weight and improved metabolic factors in overweight participants. We hypothesized that kimchi and its fermented form would have beneficial effects on glucose metabolism in patients with prediabetes., Methods: A total of 21 participants with prediabetes were enrolled. During the first 8 weeks, they consumed either fresh (1-day-old) or fermented (10-day-old) kimchi. After a 4-week washout period, they switched to the other type of kimchi for the next 8 weeks., Results: Consumption of both types of kimchi significantly decreased body weight, body mass index, and waist circumference. Fermented kimchi decreased insulin resistance, and increased insulin sensitivity, QUICKI and disposition index values (p = 0.004 and 0.028, respectively). Systolic and diastolic blood pressure (BP) decreased significantly in the fermented kimchi group. The percentages of participants who showed improved glucose tolerance were 9.5 and 33.3% in the fresh and fermented kimchi groups, respectively., Conclusions: Consumption of kimchi had beneficial effects on glucose metabolism-related and anthropometric factors in participants with prediabetes. Fermented kimchi had additional effects on BP and insulin resistance/sensitivity. The percentage of participants who showed improvement in glucose tolerance was high in the fermented kimchi group., (© 2013 S. Karger AG, Basel.)

We investigated the effects of fibroblast growth factor-21 (FGF-21) on palmitate-induced insulin resistance in skeletal muscle myotubes. First, to determine the effect of FGF-21 on palmitate-induced insulin resistance, we measured 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-d-glucose uptake and levels of proteins involved in insulin signaling pathways (IRS-1 and Akt) in human skeletal muscle myotubes (HSMMs) exposed to palmitate for 24h, and compared HSMMs exposed to palmitate and different doses of recombinant FGF-21. Second, to determine the mechanisms underlying the contribution of FGF-21 to palmitate-induced insulin resistance, we compared levels of proteins linked to palmitate-induced insulin resistance (PKC-θ, IKKα/β, JNK, p38, IκBα, and NF-κB) in HSMMs exposed to palmitate and different doses of recombinant FGF-21 for 24h. Palmitate-reduced glucose uptake was restored by FGF-21. Palmitate inhibited phosphorylation of Akt and thereby impaired insulin signaling in HSMMs. FGF-21 prevented palmitate from inhibiting the phosphorylation of Akt. These results indicate that FGF-21 prevented palmitate-induced insulin resistance in HSMMs. Palmitate activated NF-κB in HSMMs, thereby impairing the action of insulin and initiating chronic inflammation. FGF-21 inhibited palmitate-induced NF-κB activation in HSMMs. The results of the present study suggest that FGF-21 prevents palmitate-induced insulin resistance in HSMMs by inhibiting the activation of stress kinase and NF-κB., (Copyright © 2012 Elsevier Inc. All rights reserved.)

The inverse-micellar preparation of Si nanoparticles (Nps) was improved by utilizing sodium naphthalide. The Si Nps were subsequently functionalized with 4-vinylbenzoic acid for their attachment onto TiO(2) films of dye-sensitized solar cells (DSSCs). The average diameter of the COOH-functionalized Si (Si-COOH) Nps was 4.6(±1.7) nm. Depth profiling by secondary-ion mass spectrometry revealed that the Si Nps were uniformly attached onto the TiO(2) films. The number of Ru(II) dye molecules adsorbed onto a TiO(2) film that was treated with the Si-COOH Nps was 42 % higher than that on the untreated TiO(2) film. As a result, DSSCs that incorporated the Si-COOH Nps exhibited higher short-circuit photocurrent density and an overall energy-conversion efficiency than the untreated DSSCs by 22 % and 27 %, respectively. This enhanced performance, mostly owing to the intramolecular charge-transfer to TiO(2) from the dye molecules that were anchored to the Si-COOH Nps, was confirmed by comparing the performance with two different Ru(II) -bipyridine dyes (N719 and N749)., (Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Aims: Fibroblast growth factor 21 (FGF21) is an important regulator of glucose/lipid metabolism. Although there are studies examining the relationship between serum FGF21 levels and glucose homeostasis, the role of FGF21 remains unclear. The objective of this study was to examine whether serum FGF21 levels are associated with metabolic parameters in subjects with varying degrees of obesity and glucose tolerance and with complications in subjects with type2 diabetes mellitus (T2DM)., Methods: The study consisted of 213 subjects who were lean and had normal glucose tolerance (lean NGT), were overweight with NGT, had impaired glucose tolerance (IGT) or had T2DM. Serum FGF21 levels and their associations with the parameters of adiposity, glucose tolerance and the presence of diabetic complications were examined., Results: The serum FGF21 levels in T2DM were higher than in lean NGT. Serum FGF21 levels showed a positive correlation with the urine albumin-to-creatinine ratio (ACR) in all subjects except for the T2DM subjects, who showed a correlation after adjustment of age, gender and body mass index. Moreover, the subjects with carotid artery plaque showed higher serum FGF21 levels than those without complications., Conclusion: Serum FGF21 levels were associated with the urine ACR and diabetic complications including carotid artery plaque., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Free fatty acids (FFAs) lead to the activation of inflammatory pathways related to the induction of insulin resistance. Visfatin is known to play a role in obesity-related metabolic diseases and inflammatory conditions. Here, the role of visfatin in FFA-induced inflammation was investigated in hepatocytes. The following factors were examined: (1) the protein and messenger RNA (mRNA) expression of visfatin in the liver tissue of insulin-resistant rats and in (2) in HepG2 cells treated with palmitate, (3) the palmitate-induced mRNA expression and protein synthesis of interleukin-6 and tumor necrosis factor-α in HepG2 cells transfected with visfatin-specific small interfering RNA, and (4) the expression of visfatin in HepG2 cells treated with a nuclear factor-κB (NF-κB) inhibitor (SN50) and infected with Ad-IκBα. The protein and mRNA levels of visfatin were significantly higher in insulin-resistant rat liver tissue compared with the control group. Visfatin expression and protein synthesis significantly increased in HepG2 cells treated with palmitate in a time- and concentration-dependent manner. Visfatin-specific small interfering RNA significantly decreased the palmitate-induced mRNA expression and protein synthesis of interleukin-6 and tumor necrosis factor-α. A NF-κB inhibitor induced the downregulation of visfatin in HepG2 cells following treatment with palmitate. HepG2 cells infected with Ad-IκBα showed decreased expression of visfatin following treatment with palmitate. The expression of visfatin is closely associated with the expression of proinflammatory cytokines in FFA-induced inflammation and is significantly decreased by NF-κB inhibition in HepG2 cells. Visfatin may play a role in FFA-induced inflammation in hepatocytes through the NF-κB pathway., (Copyright © 2011 Elsevier Inc. All rights reserved.)

A dye-sensitized solar cell (DSSC) containing a TiO(2) film treated with COOH-functionalized germanium nanoparticles (Ge-COOH Nps) exhibited a higher short-circuit photocurrent density (J(sc); 15.4 mA cm(-2)) compared to the corresponding untreated DSSC (13.4 mA cm(-2)) using N719 and a 12 μm thick TiO(2) film at 100 mW cm(-2). The amount of N719 attached to the treated TiO(2) film was 21% greater than that attached to the untreated TiO(2) film. Enhancement of the J(sc) value by 15% was attributed mostly to an intramolecular charge transfer from N719 attached to the Ge-COOH Nps to the TiO(2) conduction band through the Ge-COOH Nps., (Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Background: The prevalence of obesity and asthma has been increasing during the last several decades. Obesity has been reported to be associated with asthma. Obesity, especially abdominal obesity, is the main component of the metabolic syndrome., Objectives: We thus hypothesized that metabolic syndrome is an important contributing factor for the development of asthma-like symptoms., Methods: The Korean Health and Genome Study started in 2001 as an ongoing population-based study of Korean adults 40 to 69 years of age. The prevalence of asthma-like symptoms in the previous 12 months was obtained by a questionnaire, and spirometric testing was conducted., Results: Among the 10,038 participants, the data from 9,942 individuals (4,716 men and 5,226 women) was available. Asthma-like symptoms (wheeze [p = 0.0006], resting dyspnea [p = 0.0062], and post-exercise dyspnea [p < 0.0001]) were increased in the subjects of the metabolic syndrome group. Subjects with asthma-like symptoms had a decreased lung function compared to subjects without asthma-like symptoms. Among the components of the metabolic syndrome, abdominal obesity and hypertension were the risk factors for asthma-like symptoms., Conclusions: Metabolic syndrome is associated with asthma-like symptoms. Among the components of metabolic syndrome, abdominal obesity and hypertension are the risk factors for asthma-like symptoms.

Background and Aim: To investigate the role of insulin signaling defects in impaired glucose tolerance (IGT), we assessed the functionality of the insulin signaling cascade before and after insulin stimulation in both IGT group and control group., Methods: Ten IGT subjects and 15 control subjects were recruited for this study. Whole-body insulin-mediated glucose uptake was determined using a euglycemic hyperinsulinemic clamp test. Muscle biopsies were obtained from the vastus lateralis muscle before and after insulin stimulation, to assess the insulin signaling cascade., Results: The insulin-stimulated incremental changes in phosphorylated IR-beta, IRS, Akt, and GSK-3 beta and in the membrane-associated PKC-zeta protein level were reduced in the IGT group compared with those in the control group (p<0.05). The membrane-associated PKC-lambda protein level was also reduced in the IGT group, but not significantly so (p=0.08). The incremental changes in the protein levels of PKC-alpha, -beta, and -theta were not significantly different between the two groups., Conclusion: The subjects with IGT showed decreased membrane-associated PKC-zeta/lambda activity in response to insulin stimulation, as well as defects in early insulin signaling. Our results suggest that membrane-associated PKC-alpha and -beta may not be associated with insulin resistance in IGT.

Oxidized LDL (OxLDL), a causal factor in atherosclerosis, induces the expression of heat shock proteins (Hsp) in a variety of cells. In this study, we investigated the role of CD36, an OxLDL receptor, and peroxisome proliferator-activated receptor gamma (PPARgamma) in OxLDL-induced Hsp70 expression. Overexpression of dominant-negative forms of CD36 or knockdown of CD36 by siRNA transfection increased OxLDL-induced Hsp70 protein expression in human monocytic U937 cells, suggesting that CD36 signaling inhibits Hsp70 expression. Similar results were obtained by the inhibition of PPARgamma activity or knockdown of PPARgamma expression. In contrast, overexpression of CD36, which is induced by treatment of MCF-7 cells with troglitazone, decreased Hsp70 protein expression induced by OxLDL. Interestingly, activation of PPARgamma through a synthetic ligand, ciglitazone or troglitazone, decreased the expression levels of Hsp70 protein in OxLDL-treated U937 cells. However, major changes in Hsp70 mRNA levels were not observed. Cycloheximide studies demonstrate that troglitazone attenuates Hsp70 translation but not Hsp70 protein stability. PPARgamma siRNA transfection reversed the inhibitory effects of troglitazone on Hsp70 translation. These results suggest that CD36 signaling may inhibit stress- induced gene expression by suppressing translation via activation of PPARgamma in monocytes. These findings reveal a new molecular basis for the anti-inflammatory effects of PPARgamma.

Objectives: Prior evidence suggests that physicians may alter process of care based on race/ethnicity. The objective of this study was to determine whether race/ethnicity predicts whether a patient receives computed tomography of the head (head CT) during evaluation of blunt head injury., Methods: This was a nonconcurrent cohort study set in an emergency department of a Level 1 trauma center in a university medical center. Consecutive patients presenting with blunt head injury from January 2000 to December 2000 were enrolled. The main outcome measure was whether or not a patient received head CT during evaluation of blunt head injury., Results: The unadjusted probability of receiving head CT was similar among minority (33.9%; 95% confidence interval [CI] = 30.0% to 38.1%) and non-Hispanic white patients (36.4%; 95% CI = 33.5% to 39.3%). After adjusting for important clinical and socioeconomic predictors, minority patients had a probability of receiving head CT 0.84 times as high as that of non-Hispanic whites, but this result was not statistically significant (95% CI = 0.67 to 1.09)., Conclusions: Minority and non-Hispanic white patients may not have significantly different rates of receiving head CT during evaluation of blunt head injury. A multicenter prospective study is necessary to confirm these preliminary findings.

Background and Aim: In vivo and in vitro experimental findings indicate that the hyperglycemic diabetic milieu can induce altered expression of the matrix metalloproteinase (MMP) genes and contribute to imbalances in vascular matrix homeostasis. We examined the plasma levels of enzymes and inhibitors involved in extracellular matrix turnover., Methods: We measured the plasma concentrations of MMP-2, MMP-9, and tissue inhibitor of metalloproteinase 1 (TIMP-1) in 80 type-2 diabetic subjects without uremia and in 80 age-matched controls. In addition, we determined the plasma levels of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and high sensitive(hs) C-reactive protein (CRP) in both groups., Results: Plasma MMP-2, TIMP-1, and hs-CRP concentrations were significantly elevated in diabetic patients as compared to the control subjects (p<0.05). Plasma levels of MMP-2, MMP-9, TIMP-1, VCAM-1, ICAM-1, and hs-CRP were found not to be significantly associated with age, duration of diabetes, blood pressure, or serum lipid concentrations., Conclusions: Plasma MMP-2, TIMP-1 and hs-CRP concentrations were significantly increased in type-2 diabetic patients.

Spatholobi Caulis has been used in Oriental medicine to treat cancer and blood stasis. In this study, the methylene chloride fraction of Spatholobi Caulis (MCSC) was examined to determine if it possesses anti-cancer activity via its apoptosis-inducing activity. MCSC exhibited a strong cytotoxic effect against human monocyte leukemia U937 cells (IC(50)=15.1 microg/ml). A TUNEL assay showed that the MCSC caused a characteristic ladder pattern of discontinuous DNA fragments and apoptotic bodies. Flow cytometric analysis confirmed that MCSC significantly increases the number of apoptotic cells stained by annexin V(+)/PI(-) cells. Western blotting revealed that MCSC activated caspase-3 expression and cleaved poly (ADP-ribose) polymerase (PARP) in a concentration-dependent manner. An enzyme-linked immunosorbent assay (ELISA) demonstrated that MCSC significantly activated the caspase-3 activity compared with the untreated control by. Taken together, these results suggest that MCSC can induce apoptosis in U937cells via the caspase dependent pathway.

Antitumor and immunomodulatory activities of an aqueous extract (GF100) of Acanthopanax senticosus were examined. In experimental lung metastasis of colon26-M3.1 carcinoma cells, intravenous (i.v.) administration of GF100 2 days before tumor inoculation significantly inhibited lung metastasis in a dose-dependent manner. The i.v. administration of GF100 also exhibited the therapeutic effect on tumor metastasis of colon26-M3.1 cells, when it was injected 1 day after tumor inoculation. In an in vitro cytotoxicity analysis, GF100 at the concentration up to 1000 microg/ml did not affect the growth of colon26-M3.1 cells. In contrast, GF100 enhanced the responsiveness to a mitogen, concanavalin A (ConA), of splenocytes in a dose-dependent manner. Peritoneal macrophage stimulated with GF100 produced various cytokines such as IL-1beta, TNF-alpha, IL-12 and IFN-gamma in an in vitro experiment. The macrophages obtained from the mice which were injected with GF100 (500 microg) 3 days before the assay showed significantly higher tumoricidal activity against tumor cells than that of the untreated macrophages. In addition, the i.v. administration of GF100 significantly augmented NK cytotoxicity to Yac-1 cells. The depletion of NK cells by injection of rabbit anti-asialo GM1 serum completely abolished the inhibitory effect of GF100 on lung metastasis of colon26-M3.1 cells. These data suggest that GF100 has antitumor activity to inhibit tumor metastasis prophylactically as well as therapeutically, and its antitumor effect is associated with activation of macrophages and NK cells.

Oral bacterium S11 was isolated from the saliva of young children without dental caries and with little or no visible supragingival plaque. The S11 strain showed 99.5% similarity with Lactobacillus fermentum, and was identified on the basis of biochemical characteristics and a 16S rDNA sequence. S11 strain and its culture supernatant significantly inhibited the formation of the insoluble glucan produced by Streptococcus mutans Ingbritt. S11 did not affect the multiplication of S. mutans Ingbritt, but the adherence of S. mutans Ingbritt onto cuvette walls was inhibited completely., (Copyright Blackwell Munksgaard, 2004.)

Previously, we reported that water-extracted Acanthopanax senticosus exhibited anti-metastatic activity by stimulating the immune system. In this study, we fractionated glycoproteins (EN-SP) from the soluble protein layer (GF-AS) of A. senticosus and determined their basic chemical properties. We also investigated the anti-tumor and immunostimulating activities of the fractionated glycoprotein, EN-SP. We found that intravenous (i.v.) administration of GF-AS dramatically inhibited metastasis of colon26-M3.1 carcinoma cells to the lung in a dose-dependent manner. In vitro analysis showed GF-AS to enhance the proliferation of splenocytes. GF-AS also stimulated peritoneal macrophage, which was followed by the production of various cytokines such as IL-1beta, TNF-alpha, IL-12 and IFN-gamma. Furthermore, the production of these cytokines was partially blocked when peritoneal macrophage was cultured with the polyclonal antibodies against GF-AS. The depletion of NK cells by rabbit anti-asialo GM1 serum partly abolished the inhibitory effect of GF-AS on lung metastasis of colon26-M3.1 cells. Using gel filtration, EN-SP, an active glycoprotein fraction, is isolated from GF-AS. While both GF-AS and EN-SP stimulated the proliferatation of splenocytes of normal mice, EN-SP showed higher anti-metastatic activity and more potently stimulated the proliferation of splenocytes compared to GF-AS. These results suggest the use of EN-SP, the fractionated glycoprotein from A. senticosus, can be used as a therapeutical reagent to prevent or inhibit tumor metastasis.

Methamphetamine (METH) causes neurotoxic damages to the dopaminergic system in mammals, but whether it exerts toxicity to dopamine cells in culture has not been fully explored. In order to develop an in vitro model of METH-induced dopamine neurotoxicity toward more systemical examination of the mechanism, we investigated METH toxicity in a clonal dopamine producing cell line (CATH.a). We show in the present study that METH produces a time- and dose-dependent increase in cell death via a process similar to apoptosis. The METH toxicity seems to be produced by oxidative stress, as it was attenuated by the antioxidant glutathione, and to involve dopamine because dopamine release and synthesis inhibitors attenuated the toxicity. This catecholaminergic cell line derived from the central nervous system may become a useful in vitro model to elucidate the mechanism underlying the METH-induced dopaminergic neuronal damage.