Total and High Molecular Weight Adiponectin and Hepatocellular Carcinoma with HCV Infection

Adiponectin is shown to be inversely associated with development and progression of various cancers. We evaluated whether adiponectin level was associated with the prevalence and histological grade of hepatocellular carcinoma (HCC), and liver fibrosis in patients with hepatitis C virus (HCV) infection.A case-control study was conducted on 97 HCC patients (cases) and 97 patients (controls) matched for sex, Child-Pugh grade and platelet count in patients with HCV infection. The serum total and high molecular weight (HMW) adiponectin levels were measured by enzyme-linked immunosorbent assays and examined in their association with the prevalence of HCC. In addition, the relationship between these adiponectin levels and body mass index (BMI), progression of liver fibrosis, and histological grade of HCC was also evaluated. Liver fibrosis was assessed using the aspartate aminotransferase to platelet ratio index (APRI).There were no significant differences in the serum total and HMW adiponectin levels between cases and controls. Moreover, there were no inverse associations between serum total and HMW adiponectin levels and BMI in both cases and controls. On the other hand, serum total and HMW adiponectin levels are positively correlated with APRI in both cases (r = 0.491, P<0.001 and r = 0.485, P<0.001, respectively) and controls (r = 0.482, P<0.001 and r = 0.476, P<0.001, respectively). Interestingly, lower serum total (OR 11.76, 95% CI: 2.97–46.66 [P<0.001]) and HMW (OR 10.24, CI: 2.80–37.40 [P<0.001] adiponectin levels were independent risk factors of worse histological grade of HCC.Our results suggested that serum total and HMW adiponectin levels were predictors of liver fibrosis, but not prevalence of HCC in patients with HCV infection. Moreover, low these adiponectin levels were significantly associated with worse histological grades

Insulin resistance and chronic liver disease

Increased insulin resistance is frequently associated with chronic liver disease and is a pathophysiological feature of hepatogenous diabetes. Distinctive factors including hepatic parenchymal cell damage, portal-systemic shunting and hepatitis C virus are responsible for the development of hepatogenous insulin resistance/diabetes. Although it remains unclear whether insulin secretion from pancreatic beta cells is impaired as it is in type 2 diabetes, retinopathic and cardiovascular risk is low and major causes of death in cirrhotic patients with diabetes are liver failure, hepatocellular carcinoma and gastrointestinal hemorrhage. Hemoglobin A1c is an inaccurate marker for the assessment and management of hepatogenous diabetes. Moreover, exogenous insulin or sulfonylureas may be harmful because these agents may promote hepatocarcinogenesis. Thus, pathogenesis, cause of death, assessment and therapeutic strategy for hepatogenous insulin resistance/diabetes differ from those for lifestyle-related type 2 diabetes. In this article, we review features of insulin resistance in relationship to chronic liver disease. We also discuss the impact of anti-diabetic agents on interferon treatment and hepatocarcinogenesis

Investigation on the Characteristics of Bottom Sediments in Tazawa-ko and Tamagawa-dam Lakes

The bottom sediments extracted in Tazawa-ko (2011.8) and Tamagawa-dam (2012.9) lakes were investigated by chemical and structural analyses. The depth profiles of silicon, aluminum and iron species suggested that the solid of the aluminum and the iron compounds, clays and zeolite minerals were distributed over the whole layer uniformly in the case of Tamagawa-dam lake, on the other hand, Al and Fe species had a lower density in the deeper segments of Tazawa-ko lake bottom sediment. Instead, accumulation of dead body of diatoms was observed in these segments

Association between total and HMW adiponectin and histological grade in patients with hepatocellular carcinoma by multiple logistic regression analysis.

<p>Abbreviation: OR = odds ratio; 95% CI = confidence interval; HMW = high molecular weigh.</p><p>Model 1: adiponectin only.</p><p>Model 2: adiponectin and covariates in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0026840#pone-0026840-t002" target="_blank">Table 2</a>.</p

Serum adiponectin levels and aspartate aminotransferase-to-platelet ratio index (APRI).

<p>A. Correlation between serum total adiponectin levels and APRI in controls (r = 0.482, <i>P</i><0.001). B. Correlation between serum high molecular adiponectin (HMW) adiponectin levels and APRI in controls (r = 0.476, <i>P</i><0.001). C. Correlation between serum total adiponectin levels and APRI in cases (r = 0.491, <i>P</i><0.001). D. Correlation between serum HMW adiponectin levels and APRI in cases (r = 0.485, <i>P</i><0.001).</p

Serum adiponectin levels and body mass index (BMI).

<p>A. Correlation between serum total adiponectin levels and BMI in controls (r = −0.142, <i>P</i> = 0.166). B. Correlation between serum high molecular adiponectin (HMW) adiponectin levels and BMI in controls (r = −0.144, <i>P</i> = 0.160). C. Correlation between serum total adiponectin levels and BMI in cases (r = −0.129, <i>P</i> = 0.208). D. Correlation between serum HMW adiponectin levels and BMI in cases (r = −0.131, <i>P</i> = 0.201).</p

Baseline clinical characteristics in case and control.

<p>Continuous variables presented as mean ± standard deviation.</p><p>Abbreviation: AST = aspartate aminotransferase; ALT = alanine aminotransferase;</p><p>APRI = aspartate aminotransferase-to-platelet ratio index; BMI = body mass index;</p><p>HMW = high molecular weigh.</p

Comparison of adiponectin levels according to histological grades in 97 cases.

<p>A. The serum total adiponectin levels in patients with moderately (<i>P</i> = 0.001) and poorly (<i>P</i><0.001) differentiated hepatocellular carcinoma (HCC) were significantly lower compared to those in patients with well-differentiated HCC. B. The serum high molecular weight (HMW) adiponectin levels in patients with moderately (<i>P</i><0.001) and poorly (<i>P</i><0.001) differentiated HCC were significantly lower compared to those in patients with well-differentiated HCC.</p