Association of epicardial adipose tissue with serum level of cystatin C in type 2 diabetes.

Accumulation of epicardial adipose tissue (EAT) is considered to be a cardiovascular risk factor independent from visceral adiposity, obesity, hypertension and diabetes. We explored the parameters related to EAT accumulation, aiming to clarify the novel pathophysiological roles of EAT in subjects with type 2 diabetes (T2DM).We examined the laboratory values, including cystatinC, and surrogate markers used for evaluating atherosclerosis. EAT was measured as the sum of the adipose tissue area, obtained by plain computed tomography scans in 208 subjects with T2DM but no history of coronary artery disease.EAT correlated positively with age, body mass index (BMI), visceral fat area, leptin, cystatin C and C-peptide, while correlating negatively with adiponectin, estimated glomerular filteration rate (eGFR) and the liver-to-spleen ratio. Multiple linear regression analysis revealed serum cystatin C (β = 0.175), leptin (β = 0.536), BMI (β = 0.393) and age (β = 0.269) to be the only parameters showing independent statistically significant associations with EAT. When cystatin C was replaced with eGFR, eGFR showed no significant correlation with EAT. In reverse analysis, serum cystatin C was significantly associated with EAT after adjustment in multivariate analysis.EAT accumulation and elevated cystatin C have been independently regarded as risk factors influencing atherosclerosis. The strong association between EAT and cystatin C demonstrated herein indicates that EAT accumulation may play an important role in Cystatin C secretion, possibly contributing to cardiometabolic risk in T2DM patients

Correlations of clinical parameters with EAT.

<p>Correlations of clinical parameters with EAT.</p

Correlations of clinical parameters with cystatin C.

<p>Correlations of clinical parameters with cystatin C.</p

<i>p</i>‑Terphenyl Derivatives from the Mushroom Thelephora aurantiotincta Suppress the Proliferation of Human Hepatocellular Carcinoma Cells via Iron Chelation

A novel 2′,3′-dihydroxy-<i>p</i>-terphenyl derivative, thelephantin O (TO), which has cancer-selective cytotoxicity, was isolated. This study investigated the underlying basis of the cytotoxicity of 2′,3′-dihydroxy-<i>p-</i>terphenyl compounds in view of their ability to chelate metal ions. FeCl₂ significantly reduced TO-induced cytotoxicity, whereas several other salts of transition metals and alkaline-earth metals did not. A structure–activity relationship study using newly synthesized <i>p</i>-terphenyl derivatives revealed that <i>o</i>-dihydroxy substitution of the central benzene ring was necessary for both the cytotoxicity and Fe²⁺ chelation of the compounds. Real-time PCR array and cell cycle analysis revealed that the TO-induced cytotoxicity was attributed to cell cycle arrest at the G1 phase via well-known cell cycle-mediated genes. The TO-induced changes in the cell cycle and gene expression were completely reversed by the addition of FeCl₂. Thus, it was concluded that Fe²⁺ chelation occurs upstream in the pivotal pathway of 2′,3′-dihydroxy-<i>p</i>-terphenyl-induced inhibition of cancer cell proliferation

Baseline characteristics of the study subjects.

<p>Baseline characteristics of the study subjects.</p

The representative image of CT image evaluating EAT.

<p>A region of interest (ROI) was manually traced along the visceral pericardium as indicated green line. A density range between -200 and -30 Hounsfield Units was used to isolate adipose tissue displayed as pink area.</p

Multiple regression analysis for EAT.

<p>Multiple regression analysis for EAT.</p

Multiple regression analysis for cystatin C.

<p>Multiple regression analysis for cystatin C.</p