Shuichi Kaneko

Kanazawa Medical University, Kanazawa, Ishikawa, Japan

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Publications (561)2581.65 Total impact

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    ABSTRACT: Purpose To identify the imaging features of hepatocellular carcinoma (HCC) associated with β-catenin mutation and their relationship to pathologic findings. Materials and Methods Institutional ethics committee approval and informed consent were obtained. One hundred thirty-eight surgically resected HCCs were analyzed in this study. Immunohistochemical expression of β-catenin and its transcriptional product, glutamine synthetase (GS), were graded and classified into three groups: the β-catenin positive and GS positive group (HCC with β-catenin mutation), the β-catenin negative and GS positive group (intermediate HCC), and the β-catenin negative and GS negative group (HCC without β-catenin mutation). Clinical, pathologic, and imaging findings from dynamic computed tomography (CT) and gadoxetic acid-enhanced magnetic resonance (MR) imaging (T1-weighted, T2-weighted, diffusion-weighted, and hepatobiliary phase imaging) were evaluated. Correlations among immunohistochemical expression of β-catenin, GS, and organic anion transporting polypeptide 1B3 (uptake transporter of gadoxetic acid) were evaluated. The χ(2), Kruskal-Wallis, and Spearman correlation tests were used. Results HCCs with β-catenin mutation (n = 27) showed a lower median contrast-to-noise ratio at diffusion-weighted imaging than did intermediate HCCs (n = 23) and HCCs without β-catenin mutation (n = 84) (13.2, 24.4, and 27.0, respectively; P = .02), higher apparent diffusion coefficient (1.33, 1.13, and 1.12, respectively; P < .0001), higher contrast-to-noise ratio (0.58, -28.7, and -45.0, respectively; P < .0001) and higher enhancement ratio during the hepatobiliary phase (0.90, 0.50, and 0.42, respectively; P < .0001). At pathologic examination, HCCs with β-catenin mutation showed pseudoglandular proliferation and bile production with a higher grade of differentiation (P = .04, .001, and .005, respectively). There were significant positive correlations among expression of β-catenin, GS, and organic anion transporting polypeptide 1B3 (P < .0001). Conclusion HCCs with β-catenin mutation showed a higher grade of differentiation with frequent pseudoglandular patterns and bile production, and characteristic imaging findings included a high enhancement ratio at gadoxetic acid-enhanced MR imaging and a high apparent diffusion coefficient at diffusion-weighted imaging. (©) RSNA, 2015 Online supplemental material is available for this article.
    Radiology 02/2015; · 6.21 Impact Factor
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    ABSTRACT: Carotid echo indexes [intima-media thickness (IMT)] are commonly used surrogate markers for cardiovascular disease; however, the impacts of chronic kidney disease (CKD) on changes in IMT are unclear. We examined associations between CKD and IMT in participants with and without type 2 diabetes through longitudinal analysis. In total, 424 subjects were enrolled in this study. IMT was measured as per carotid echo indexes. Relationships between IMT and risk factors were analyzed using multiple linear regression analysis, in which we defined IMT as the dependent variable and atherosclerosis-related factors (age, sex, systolic pressure, total cholesterol, body mass index, estimated glomerular filtration rate (eGFR), uric acid, smoking index, number of antihypertensive drugs, statin use, urinary protein levels, past cardiovascular event, glycated hemoglobin, and diabetes duration) as independent variables. The study population was composed of 70.3 % male subjects. Participants with diabetes accounted for 64.4 % of the total population. The mean follow-up duration was 2.2 ± 1.5 years. Alterations in IMT tended to be associated with systolic blood pressure (+10 mmHg) (β = -0.0084, p = 0.09) and eGFR (+10 mL/min/1.73 m(2)) (β = -0.0049, p = 0.06) in all participants. In participants without diabetes, alterations in IMT were associated with eGFR (+10 mL/min/1.73 m(2)) (β = -0.0104, p = 0.03) and tended to be associated with systolic blood pressure (+10 mmHg) (β = 0.0094, p = 0.06). No significant relationships were found in participants with diabetes. Low eGFR was associated with progression of carotid thickness independent of common cardiovascular risk factors in non-diabetic participants.
    Clinical and Experimental Nephrology 02/2015; · 1.71 Impact Factor
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    ABSTRACT: Excessive hepatic lipid accumulation promotes macrophages/Kupffer cells activation, resulting in exacerbation of insulin resistance and progression of non-alcoholic steatohepatitis (NASH). However, few promising treatment modalities target lipotoxicity-mediated hepatic activation/polarization of macrophages for NASH. Recent epidemiological surveys showed that serum β-cryptoxanthin, an antioxidant carotenoid, was inversely associated with the risks of insulin resistance and liver dysfunction. In the present study, we first showed that β-cryptoxanthin administration ameliorated hepatic steatosis in high-fat diet-induced obese mice. Next, we investigated the preventative and therapeutic effects of β-cryptoxanthin using a lipotoxic model of NASH: mice fed a high-cholesterol and high-fat diet ("CL diet"). After 12 weeks of CL diet feeding, β-cryptoxanthin administration attenuated insulin resistance and excessive hepatic lipid accumulation and peroxidation, with increases in M1-type macrophages/Kupffer cells and activated stellate cells, and fibrosis in CL diet-induced NASH. Comprehensive gene expression analysis showed that β-cryptoxanthin downregulated macrophage activation signal-related genes significantly without affecting most lipid metabolism-related genes in the liver. Importantly, flow cytometry analysis revealed that, on a CL diet, β-cryptoxanthin caused a predominance of M2 over M1 macrophage populations, in addition to reducing total hepatic macrophage and T cell contents. In parallel, β-cryptoxanthin decreased lipopolysaccharide-induced M1 marker mRNA expression in peritoneal macrophages, whereas it augmented IL-4-induced M2 marker mRNA expression, in a dose-dependent manner. Moreover, β-cryptoxanthin reversed steatosis, inflammation, and fibrosis progression in pre-existing NASH in mice. In conclusion, β-cryptoxanthin prevents and reverses insulin resistance and steatohepatitis, at least in part, through an M2-dominant shift in macrophages/Kupffer cells in a lipotoxic model of NASH.
    Endocrinology 01/2015; · 4.72 Impact Factor
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    ABSTRACT: The 3rd version of Clinical Practice Guidelines for Hepatocellular Carcinoma was revised by the Japan Society of Hepatology, according to the methodology of evidence-based medicine, which was published in October 2013 in Japanese. Here, we briefly describe new or changed recommendations with a special reference to the two algorithms for surveillance, diagnosis, and treatment. © 2015 The Japan Society of Hepatology.
    Hepatology research : the official journal of the Japan Society of Hepatology. 01/2015; 45(2).
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    ABSTRACT: Calciphylaxis is a life-threatening complication of end-stage kidney disease (ESKD) and leads to cutaneous necrosis and gangrene. Various risk factors for calciphylaxis have been reported, and warfarin therapy is a particularly strong trigger. Here we report the case of 50-year-old woman with ESKD and systemic lupus erythematosus who developed calciphylaxis after anti-thrombotic therapy, including warfarin, for ischemic skin ulcers due to arteriosclerosis obliterans and anti-phospholipid antibody syndrome. Although warfarin improved the thrombotic skin ulcers, it might also be a trigger for calciphylaxis. Discontinuation of the warfarin and the addition of low-density lipoprotein apheresis and sodium thiosulfate infusion failed to improve the gangrene; eventually, her legs had to be amputated to prevent lethal infection. The histology of the dermal and soft tissue obtained from the amputated legs showed typical findings of calciphylaxis. Warfarin is a vitamin K antagonist with inhibitory effects on the calcification of regulatory proteins, such as matrix Gla protein and fetuin-A. Therefore, the warfarin therapy might have induced calciphylaxis in our patient.
    CEN Case Reports. 12/2014;
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    ABSTRACT: Cytopenia during interferon-based (IFN-based) therapy for chronic hepatitis C (CHC) often necessitates reduction of doses of drugs and premature withdrawal from therapy resulting in poor response to treatment. To identify genetic variants associated with IFN-induced neutropenia, we conducted a genome-wide association study (GWAS) in 416 Japanese CHC patients receiving IFN-based therapy. Based on the results, we selected 192 candidate single nucleotide polymorphisms (SNPs) to carry out a replication analysis in an independent set of 404 subjects. The SNP rs2305482, located in the intron region of the PSMD3 gene on chromosome 17, showed a strong association when the results of GWAS and the replication stage were combined (OR = 2.18, P = 3.05 × 10(-7) in the allele frequency model). Logistic regression analysis showed that rs2305482 CC and neutrophil count at baseline were independent predictive factors for IFN-induced neutropenia (OR = 2.497, P = 0.0072 and OR = 0.998, P < 0.0001, respectively). Furthermore, rs2305482 genotype was associated with the doses of pegylated interferon (PEG-IFN) that could be tolerated in hepatitis C virus genotype 1-infected patients treated with PEG-IFN plus ribavirin, but not with treatment efficacy. Our results suggest that genetic testing for this variant might be useful for establishing personalized drug dosing in order to minimize drug-induced adverse events.
    Human Genetics 12/2014; · 4.52 Impact Factor
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    ABSTRACT: We thank Dr. Tapan and Sertoglu for their interest in our study and their comments. In the letter to the Editor, they recommend to measure fatty acid composition after excluding patients with type 2 diabetes mellitus (T2DM) because the activity of the desaturase enzymes regulating especially polyunsaturated fatty acids can be affected by T2DM and correlates with the level of fasting plasma glucose and insulin resistance [1]. In our study, HbA1c levels are 7.1±0.2% and 7.1±0.3% for simple steatosis (SS) and non-alcoholic steatohepatitis (NASH) groups, respectively, and the patients with T2DM are included in both SS and NASH groups. The number of patients with T2DM was 42/63 (66.7%) and 29/40 (72.5%) for SS and NASH groups, respectively, and there was no statistically significant difference in the rate of T2DM between SS and NASH groups. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Liver international: official journal of the International Association for the Study of the Liver 12/2014; · 4.41 Impact Factor
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    ABSTRACT: Background Selenoprotein P (SeP), a selenium-rich extracellular glycoprotein, is the primary selenoprotein in the plasma. SeP plays an important role in the maintenance of selenium levels in the peripheral tissues. We developed a new sol particle homogeneous immunoassay (SPIA) for measuring full-length SeP (FL-SeP) levels in the human serum.Methods We used colloidal gold particles coated with two types of anti-SeP monoclonal antibodies, one recognizing the N-terminal side domain of SeP and the other recognizing the C-terminal side domain.ResultsThe assay range was 0.2–9 mg/l, and the linearity was excellent. The within-day and between-day coefficients of variation ranged from 0.73% to 2.24% and 0.45% to 1.11%, respectively. Serum samples (n = 200) were examined using the newly developed assay system (employing a Model 7070 Hitachi automatic clinical analyzer) and the conventional enzyme-linked immunosorbent assay. These two methods were compared using the Passing–Bablok regression analysis; the resulting regression equation and correlation coefficient were y = 0.940x + 0.165 and r = 0.954, respectively.Conclusions Our new SPIA assay is a fully automated homogeneous immunoassay that can be used in conjunction with various commercial analyzers. The assay was sensitive, precise, and suitable for clinical measurement of the FL-SeP in the human serum.
    Journal of Clinical Laboratory Analysis 12/2014; · 1.14 Impact Factor
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    ABSTRACT: Veno-occlusive disease/sinusoidal obstruction syndrome (VOD/SOS) occurring after liver transplantation is a relatively rare complication but it often takes a life-threatening course. However, the detailed etiology and mechanism of VOD/SOS after liver transplantation (LT) remains unclear. We report two cases with rapidly progressive VOD/SOS after ABO-identical LT resistant to various therapies. In case 1, in which the patient underwent deceased-donor LT, the first episode of acute allograft rejection was triggered VOD/SOS, and the presence of donor non-specific anti-HLA antibodies was confirmed. The recipient died with graft failure on day 46 after transplantation. Case 2, in which the patient underwent living-donor LT from the mother, had neither rejection nor mechanical venous obstruction, but condition of the patient rapidly worsened and he died on day 13 after transplantation. This recipient's direct cross-match test for the donor's B lymphocyte was strongly positive, but that for T lymphocyte was negative. In both cases, neither stenosis of hepatic vein outflow tract nor C4d deposition in post-transplantation liver biopsy specimens and autopsy specimen was found. On the other hand, in both cases, the patient was transfusion unresponsive thrombocytopenia and hyperbilirubinemia persisted postoperatively, and glycoprotein Ⅰ bα was strongly stained in the neighboring centrilobular area (zone 3), especially in the space of Disse, and platelet phagocytosis was observed in Kupffer cells and hepatocytes around zone 3 such as clinical xenotransplantation of the liver in post-transplantation liver biopsy specimens. From the viewpoint of graft injury, VOD/SOS was considered that sustained sinusoidal endothelial cells injury resulted in bleeding in the space of Disse and led to around centrilobular hemorrhagic necrosis, and the fundamental cause was damage around centrilobular area including sinusoid by acute cellular rejection, antibody-mediated rejection or ischemic reperfusion injury. The extrasinusoidal platelet activation, aggregation, and phagocytosis of platelets were some of the main reasons for VOD/SOS and transfusion-resistant thrombocytopenia. Copyright © 2014 Elsevier Inc. All rights reserved.
    Transplantation Proceedings 12/2014; 46(10):3523-35. · 0.95 Impact Factor
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    ABSTRACT: The liver has robust regenerative potential in response to damage, but hepatic steatosis weakens this potential. We found that the enhanced integrated stress response (ISR) mediated by phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF2α) impairs regeneration in hepatic steatosis and that growth arrest and DNA damage-inducible 34 (Gadd34)-dependent suppression of ISR plays a crucial role in fatty liver regeneration. Although the mice fed an HFD for 2 weeks developed moderate fatty liver with no increase in eIF2α phosphorylation before 70% hepatectomy, they showed impaired liver regeneration due to reduced proliferation and increased death of hepatocytes with increased phosphorylation of eIF2α and ISR. An increased ISR through Gadd34 knockdown induced C/EBP homologous protein (CHOP)-dependent apoptosis and receptor-interacting protein kinase 3-dependent necrosis, resulting in increased hepatocyte death during fatty liver regeneration. Further, Gadd34 knockdown and increased phosphorylation of eIF2α decreased cyclin D1 protein and reduced hepatocyte proliferation. In contrast, enhancement of Gadd34 suppressed phosphorylation of eIF2α and reduced CHOP expression and hepatocyte apoptosis without affecting hepatocyte proliferation, clearly improving fatty liver regeneration. In more severe fatty liver of leptin receptor-deficient db/db mice, forced expression of hepatic Gadd34 also promoted hepatic regeneration after hepatectomy. Conclusion: Gadd34-mediated regulation of ISR acts as a physiological defense mechanism against impaired liver regeneration due to steatosis and is thus a possible therapeutic target for impaired regeneration in hepatic steatosis. This article is protected by copyright. All rights reserved. Copyright © 2014 by the American Association for the Study of Liver Diseases.
    Hepatology 11/2014; · 11.19 Impact Factor
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    ABSTRACT: Aim: Inflammation plays a critical role in cancer. The aim of the present study was to investigate the impact of neutrophil to lymphocyte ratio (NLR) on patients with advanced hepatocellular carcinoma (HCC) treated by hepatic arterial infusion chemotherapy (HAIC). Methods: We retrospectively evaluated 266 patients with advanced HCC treated by HAIC between March 2003 and December 2012. NLR was calculated from the differential leukocyte count by dividing the absolute neutrophil count by the absolute lymphocyte count. Results: The cut-off level of NLR was set as the median value of 2.87 among all patients in this study. The objective response rate in the patients with low NLR was 37.6%, which was significantly better than that of the patients with high NLR (21.1%; P<0.01). Multivariate analysis revealed that low NLR remained associated with the response to HAIC (P=0.024). Median progression-free survival and median overall survival in patients with high NLR were 3.2 months and 8.0 months, which were significantly shorter than that of the patients with low NLR (5.6 months and 20.7 months; P<0.01 and P<0.01, respectively). High NLR was an independent unfavorable prognostic factor in multivariate analysis. The patient outcome was stratified more clearly by NLR calculated after HAIC added to calculations before HAIC. Serum PDGF-BB level was positively correlated with NLR. Conclusions: The present study results suggested that NLR was a useful predictor in patients with advanced hepatocellular carcinoma treated by HAIC. These findings may be useful in determining treatment strategies or in designing clinical chemotherapy trials in future.
    Hepatology Research 10/2014; · 2.07 Impact Factor
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    ABSTRACT: Aims/IntroductionSeveral studies have indicated that statins suppress the progression of diabetic nephropathy. However, few reports have directly compared the renoprotective effects between potent and conventional statins.Materials and Methods Patients with diabetic nephropathy, selected as those with serum creatinine level of 0.9-1.5 mg/dL and simultaneously having either microalbuminuria or positive proteinuria, were randomly assigned to one of three groups: a conventional diet therapy group, a group administered 10 mg of pravastatin, and a group administered 10 mg of atorvastatin. Renal function was evaluated before and after a 12-month period of therapy.ResultsThe atorvastatin group had a significant decrease in low-density lipoprotein cholesterol (LDL-C) at 3 months and thereafter compared with the other groups. The urinary albumin/Cr ratio significantly decreased in the atorvastatin group; the degree of this decrease was significantly greater than that in the diet therapy group. The kidney function estimated with cystatin C (CysC) and the estimated glomerular filtration rate (eGFR) calculated from CysC were significantly preserved in the atorvastatin group compared with the pravastatin group. In a multivariate regression analysis, the use of atorvastatin was the only explanatory variable for the changes in CysC; this was independent of changes in LDL-C.Conclusions Atorvastatin is more effective than pravastatin for the prevention of increase in CysC, and this renoprotective effect was considered to be due to the pleiotropic effect of atorvastatin independent of its lipid-lowering effect. This study was registered with UMIN (no. UMIN 000001774).This article is protected by copyright. All rights reserved.
    Journal of Diabetes Investigation. 10/2014;
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    ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is closely related to insulin resistance and lipid metabolism. Recent studies have suggested that the quality of fat accumulated in the liver is associated with the development of nonalcoholic steatohepatitis (NASH). In this study, we investigated the fatty acid composition in liver tissue and its association with the pathology in NAFLD patients.
    Liver international: official journal of the International Association for the Study of the Liver 09/2014; · 4.41 Impact Factor
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    ABSTRACT: This study examined the effects of peretinoin, an acyclic retinoid, on the survival of patients with hepatitis C virus-related hepatocellular carcinoma (HCC) who had completed curative therapy and participated in a randomized, placebo-controlled trial.
    Journal of Gastroenterology 09/2014; · 4.02 Impact Factor
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    ABSTRACT: IntroductionA step-up strategy for dipeptidyl peptidase (DPP)-4 inhibitor-based regimens has not yet been established. In addition, similarities and differences between DPP-4 inhibitors and glucagon-like peptide (GLP)-1 receptor agonists remain to be elucidated in humans. We investigated the pleiotropic effects of vildagliptin vs liraglutide in patients with type 2 diabetes on sitagliptin-based regimens in an open-label, randomized, clinical trial.Materials and MethodsA total of 122 patients with type 2 diabetes that was inadequately controlled by sitagliptin-based regimens were randomly assigned to either vildagliptin (50 mg, twice daily) or liraglutide treatment (0.9 mg, once daily) for 12 weeks. The primary outcomes were glycated hemoglobin and body mass index.ResultsBoth vildagliptin and liraglutide significantly lowered glycated hemoglobin within 12 weeks after switching from sitagliptin, but liraglutide produced a greater reduction (−0.67 ± 0.12% vs −0.36 ± 0.53%). Liraglutide lowered body mass index, whereas vildagliptin did not affect body mass index. Vildagliptin lowered fasting C-peptide immunoreactivity, but liraglutide did not. Vildagliptin increased serum levels of adiponectin, arachidonic acid, eicosapentaenoic acid and docosahexaenoic acid, whereas liraglutide had no effect on these levels. Quality of life, assessed using the diabetes treatment satisfaction questionnaire, was not impaired in either group. The most common adverse events were gastrointestinal symptoms, which occurred with similar frequencies in both groups.Conclusions Vildagliptin-mediated improvements in glycemic control did not correlate with indices for insulin secretion and insulin sensitivity. Switching from sitagliptin to liraglutide is useful in managing hyperglycemia and weight. Each agent exerts unique pleiotropic effects. This trial was registered with the University Hospital Medical Information Network Clinical Trials Registry (no. 000004953).
    Journal of Diabetes Investigation. 09/2014;
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    ABSTRACT: Background & aimsThe aim of the present study is to evaluate the factors influencing biochemical response to treatment and the value of biochemical response for predicting long-term outcomes in Japanese patients with PBC.Patients and Methods Biochemical response to ursodeoxycholic acid (UDCA) or UDCA plus bezafibrate was defined as good (≤ULN), fair (≤1.5 x ULN), or poor (>1.5 x ULN) at 2 years after initiation of UDCA treatment. Associations between various factors (including age, sex, autoantibody status, and histological variables at baseline), biochemical response to treatment, and long-term outcomes were evaluated in 164 Japanese PBC patients.ResultsAnti-gp210 positivity and a higher bile duct loss score were significant risk factors for worse ALP response (OR, 2.78 and 1.85, respectively). Age, anti-gp210 positivity, and anti-centromere positivity were significant risk factors for worse ALT response (OR, 1.05, 4.0, and 2.77, respectively). Anti-gp210 positivity and a higher hepatitis score were significant risk factors for worse IgM response (OR, 2.10 and 2.06, respectively). Worse ALP and IgM response were significant risk factors for progression to late-stage disease without jaundice (OR, 2.27 and 2.32, respectively). Worse ALT response was a significant risk factor for progression to late-stage disease with persistent jaundice (OR, 11.11).Conclusions Biochemical response to treatment at 2 years, which is influenced by autoantibody status and histological variables at baseline, can predict long-term outcomes in Japanese patients with PBC.
    Hepatology Research 09/2014; · 2.07 Impact Factor
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    ABSTRACT: Aims/IntroductionTo examine the association between liver histological features and organ-specific insulin resistance indices calculated from 75-g oral glucose tolerance test data in patients with non-alcoholic fatty liver disease.Materials and Methods Liver biopsy specimens were obtained from 72 patients with non-alcoholic fatty liver disease, and were scored for steatosis, grade and stage. Hepatic and skeletal muscle insulin resistance indices (hepatic insulin resistance index and Matsuda index, respectively) were calculated from 75-g oral glucose tolerance test data, and metabolic clearance rate was measured using the euglycemic hyperinsulinemic clamp method.ResultsThe degree of hepatic steatosis, and grade and stage of non-alcoholic steatohepatitis were significantly correlated with Matsuda index (steatosis r = −0.45, P < 0.001; grade r = −0.54, P < 0.001; stage r = −0.37, P < 0.01), but not with hepatic insulin resistance index. Multiple regression analyses adjusted for age, sex, body mass index and each histological score showed that the degree of hepatic steatosis (coefficient = −0.22, P < 0.05) and grade (coefficient = −0.40, P < 0.01) were associated with Matsuda index, whereas the association between stage and Matsuda index (coefficient = −0.07, P = 0.593) was no longer significant. A similar trend was observed for the association between steatosis and metabolic clearance rate (coefficient = −0.62, P = 0.059).Conclusions Liver steatosis is associated with insulin resistance in skeletal muscle rather than in the liver in patients with non-alcoholic fatty liver disease, suggesting a central role of fatty liver in the development of peripheral insulin resistance and the existence of a network between the liver and skeletal muscle.
    Journal of Diabetes Investigation. 09/2014;
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    ABSTRACT: Graphical abstract We synthesized two peroxidovanadium(V) complexes (pVs) which showed insulin-mimetic activities. We examined the signal transduction pathways induced by these compounds and found the reactive oxygen species (ROS) generation from these compounds. The ROS generated by these compounds induced the signal transduction pathway which resulted in the cell survival/death pathway.
    Inorganica Chimica Acta 08/2014; 420:53–59. · 2.04 Impact Factor

Publication Stats

10k Citations
2,581.65 Total Impact Points

Institutions

  • 1994–2014
    • Kanazawa Medical University
      • • Department of Gastroenterology
      • • Department of Internal Medicine (III)
      Kanazawa, Ishikawa, Japan
  • 1987–2014
    • Kanazawa University
      • • Department of Disease Control and Homeostasis
      • • Department of Gastroenterology
      • • Department of Internal Medicine
      • • Division of Oncology and Molecular Biology
      • • School of Medicine
      Kanazawa, Ishikawa, Japan
  • 2013
    • University of North Carolina at Chapel Hill
      North Carolina, United States
  • 2006–2013
    • The University of Tokyo
      • Institute of Industrial Science
      Tōkyō, Japan
    • Kumamoto University
      • Department of Reproductive Engineering
      Kumamoto, Kumamoto Prefecture, Japan
  • 2012
    • National Center for Global Health and Medicine in Japan
      Tiba, Chiba, Japan
  • 2011
    • Musashino Red Cross Hospital
      Edo, Tōkyō, Japan
  • 2010
    • Çanakkale Onsekiz Mart Üniversitesi
      Kale-Sultanie, Çanakkale, Turkey
  • 2004–2010
    • Jichi Medical University
      • Division of Clinical Pharmacology
      Totigi, Tochigi, Japan
  • 2008
    • NEC Corporation
      Edo, Tōkyō, Japan
  • 2007
    • University Hospital Medical Information Network
      Edo, Tōkyō, Japan
  • 2002
    • Nagai Internal Medicine Clinic
      Okayama, Okayama, Japan
  • 2001
    • Kanazawa Municipal Hospital
      Kanazawa, Ishikawa, Japan
  • 2000
    • Osaka University
      • Division of Cellular and Molecular Biology
      Ibaraki, Osaka-fu, Japan
  • 1994–1997
    • Kanazawa Institute of Technology
      Kanazawa, Ishikawa, Japan
  • 1995
    • University of Southern California
      Los Angeles, California, United States
  • 1989–1994
    • National Institute of Allergy and Infectious Diseases
      • Laboratory of Immunoregulation
      Maryland, United States