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CDTect-RIA and CDTect-EIA for determination of serum carbohydrate-deficient transferrin (CDT) by radioimmunossay and enzyme immunoassay respectively were tested for equality and precision in four European laboratories. For correlational studies, serum samples with CDT concentrations up to 130 U/I were analysed in accordance with a uniform trial schedule. The regression of CDT values obtained by the two procedures was computed for each laboratory using the method of Passing and Bablok. Slopes and intercepts of the regression functions did not differ significantly from the values 1 or 0, as proved by the corresponding 95% confidence intervals. Precision studies were computed using analysis of variance. For CDT concentrations at the upper reference limit for men, the within-day coefficients of variation (CVs) ranged between 0.7 and 6.4% (median 5.2%) for CDTect-RIA and from 4.3 to 9.2% (median 6.2%) for CDTect-EIA. The corresponding pure between-day CVs were 5.0-18.5% (median 9.8%) and 3.5-14.5% (median 10.9%). The study demonstrates the equality of CDT values obtained by CDTect-RIA and CDTect-EIA. According to this study, the two methods can be used interchangeably without getting fluctuating CDT values, e.g. in longitudinal studies. [ABSTRACT FROM PUBLISHER]

Adiponectin is an insulin-sensitizing, antiatherogenic and antiinflammatory adipocytokine that circulates in plasma in three isoforms: a trimer (low-molecular weight (LMW)), a hexamer (trimer-dimer) of medium-molecular weight (MMW) and a multimeric high-molecular weight (HMW) isoform. Evidence suggests that HMW adiponectin is the active isoform the adipocytokine. We investigated the impact of adipose tissue and insulin sensitivity on adiponectin isoform distribution. Altogether 187 normolipidemic, non-diabetic, female and male, lean and obese subjects with and without insulin resistance participating in the Salzburg Atherosclerosis Prevention program in subjects at High Individual Risk (SAPHIR) were included in the study. Insulin sensitivity was determined by the short insulin tolerance test and the homeostasis model assessment (HOMA) index. Serum adiponectin isoform distribution was determined by ELISA. Total adiponectin as well as HMW/total adiponectin ratio was significantly increased in female subjects. Circulating adiponectin declined with raising body mass index due to reductions in HMW isoform. As determined by stepwise regression analysis, besides age and HDL cholesterol, amount of visceral adipose tissue and waist-to-hip ratio predicted concentration of HMW adiponectin, while insulin sensitivity had no influence on either total adiponectin or its isoforms. Our data suggest that the HMW isoform of adiponectin is a more sensitive marker of cardiovascular risk than total adiponectin concentration. Visceral adipose tissue mass - but not insulin sensitivity - is a strong determinant of adiponectin secretion so that we hypothesize that insulin resistance is rather a consequence than the cause of hypoadiponectinemia in obese subjects. [ABSTRACT FROM AUTHOR]

Pronounced weight loss was shown to improve adipocyte dysfunction and insulin sensitivity in obese subjects. While bariatric surgery is frequently accompanied by adverse side effects, weight loss due to caloric restriction is often followed by weight regain. Here we aimed to determine whether switching the diet from a metabolically harmful Western type diet to a balanced standard diet is sufficient to reverse adipocyte dysfunction in diet-induced obese mice. Male C57BL/6 mice were fed a Western diet for 10 weeks and afterwards switched to a standard diet for eight more weeks (WD/SD mice) or continued to be fed a Western diet (WD/WD mice) ad libitum. Mice fed SD for 18 weeks served as control group (SD/SD). Insulin sensitivity was similar in WD/SD and SD/SD mice despite increased body weight in WD/SD mice. Beiging markers Ucp-1, Cidea and Cox8b were drastically reduced in subcutaneous adipose tissue of WD/SD mice when compared with SD/SD mice. Also, in brown adipose tissue morphologic features and markers of thermogenesis were still altered in both WD/SD and WD/WD mice. However, adipocyte size, Hif1α and macrophage infiltration were significantly lower in both, brown and white adipose tissues of WD/SD compared to WD/WD mice and additionally, a shift toward anti-inflammatory M2 phenotype was found in WD/SD mice only. In conclusion our data suggest that switching the diet is sufficient to improve adipose tissue inflammation, while western diet negatively affects thermogenic capacity of brown adipose tissue, and inhibits beiging of white adipose tissue in the long-term. [ABSTRACT FROM AUTHOR]