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Context: T-cadherin (T-cad) is a glycosylphosphatidylinositol (GPI)-anchored cadherin that mediates adiponectin to induce exosome biogenesis and secretion, protect cardiovascular tissues, promote muscle regeneration, and stimulate therapeutic heart protection by transplanted mesenchymal stem cells. CDH13, the gene locus of T-cad, affects plasma adiponectin levels most strongly, in addition to affecting cardiovascular disease risk and glucose homeostasis. Recently, it has been suggested that T-cad exists in human serum, although the details are still unclear.Objective: To validate the existence of T-cad forms in human serum and investigate the association with clinical parameters of type 2 diabetes patients.Methods: Using newly developed monoclonal antibodies against T-cad, pooled human serum was analyzed, and novel T-cad enzyme-linked immunosorbent assays (ELISAs) were developed. The serum T-cad concentrations of 183 Japanese type 2 diabetes patients were measured in a cross-sectional observational study. The main outcome measure was the existence of soluble T-cad in human serum.Results: There were 3 forms of soluble T-cad: a 130-kDa form with a prodomain, a 100-kDa mature form, and a 30-kDa prodomain in human serum. Using newly developed ELISAs to measure them simultaneously, we found that the 130-kDa form of T-cad positively correlated with plasma adiponectin (r = 0.28, P < .001), although a physiological interaction with adiponectin was not observed in serum. The unique 30-kDa prodomain was associated with several clinical parameters in diabetes patients.Conclusion: We identified 3 novel forms of soluble T-cad. Their importance as disease markers and/or biomarkers of adiponectin function and the possible bioactivity of the respective molecules require further investigation. [ABSTRACT FROM AUTHOR]

Measurements of glycated albumin (GA) as well as glycated haemoglobin (HbA1C) have been applied in order to monitor chronic glycemic control in diabetic patients. Since the levels of both glycated proteins are influenced by various factors other than glycemia, cautions are necessary to evaluate such measures in some specific conditions. In this study, we examined the effects of serum uric acid (UA) levels on these glycemic markers. One hundred and ninety-three men with normal glucose tolerance were enrolled in this study. Association of serum UA with BMI, plasma glucose (PG), high sensitivity CRP (hs-CRP), serum GA and HbA1C was analysed. Serum UA showed a significant positive correlation with BMI ( R = 0.329, P < 0.0001) and hs-CRP ( R = 0.306, P < 0.0001). Multivariate analysis revealed serum UA to be a significant positive explanatory variable for hs-CRP. There was a significant positive correlation of serum UA with the 2-h PG after 75 g OGTT but not fasting PG. Although there was no correlation of serum UA with HbA1C, serum UA showed a significant inverse correlation with both serum GA ( R = −0.402, P < 0.0001) as well as BMI-adjusted serum GA ( R = −0.327, P < 0.0001). By multivariate analysis, serum UA was an explanatory variable for serum GA. Serum GA, but not HbA1C, is set lower in relation to plasma glucose levels in hyperglycemic men. This may be caused by microinflammation associated with hyperuricemic state. [ABSTRACT FROM AUTHOR]

Abstract: Glycated albumin (GA) is a new glycemic control indicator. GA/HbA1c ratio in autoimmune acute-onset type 1 diabetes mellitus patients was significantly higher than in type 2 diabetes mellitus patients at the time of diagnosis. This difference might reflect speed of increase in plasma glucose after the onset of diabetes. [Copyright &y& Elsevier]

Abstract: Background: In patients with hemolytic anemia (HA), glycated hemoglobin (HbA1C) presents lower values in relation to glycemia because the lifespan of erythrocytes is shortened, whereas glycated albumin (GA) is not affected. In the present study, we examined the usefulness of GA as an indicator of glycemic control status in patients with HA. Methods: We enrolled 21 patients with HA. A total of 202 patients with type 2 diabetes mellitus (T2DM) without complications were used as controls. Results: We identified a significant correlation between GA and HbA1C in the patients with HA. However, in a comparison between the patients with HA and those with T2DM, the regression line showed a leftward shift in the former group. There was a significant positive correlation between hemoglobin (Hb) and HbA1C in the patients with HA (R=0.541, p=0.025), although there was no significant correlation between Hb and GA. There was an inverse correlation between Hb levels and GA/HbA1C ratio (R=−0.710, p=0.001). The measured HbA1C levels were lower than the HbA1C levels estimated from mean plasma glucose levels, whereas the GA/3 levels were close to the estimated HbA1C levels. Conclusions: GA is a useful indicator of glycemic control status in patients with HA. [Copyright &y& Elsevier]