Correlations between plasma omentin-1 levels and anthropometric, plasma, hemodynamic parameters, and cardiac dimensions and function.

<p>Data are Pearson’s r. In case of non-Gaussian distributions, parameters were ln-transformed for correlation analysis. A, diastolic atrial contraction; BMI, body mass index; DM2, type 2 diabetes; E, early diastolic filling phase; HbA1c, glycated hemoglobin; HDL, high-density lipoprotein; LV, left ventricular; MFAE, myocardial fatty acid esterification; MFAO, myocardial fatty acid oxidation; MFAU, myocardial fattu acid uptake; MMRGlu, myocardial metabolic glucose metabolism; M-value, whole body insulin sensitivity.</p>#<p><i>P</i><0.10;</p>*<p><i>P</i><0.05;</p>**<p><i>P</i><0.01;</p>***<p><i>P</i><0.001.</p

Characteristics of subjects for determination of circulating omentin-1 levels.

<p>Data are mean ± SD or median (interquartile range). <i>P</i>-values for differences between variables were calculated using the students <i>t</i>-test in case of normally distributed data, or the Mann-Whitney U-test in case of non-Gaussian distributions data.</p>***<p>indicates <i>P</i><0.001;</p>**<p><i>P</i><0.01;</p>*<p><i>P</i><0.05;</p>#<p><i>P</i><0.10. A, diastolic atrial contraction; BMI, body mass index; DM2, type 2 diabetes; E, early diastolic filling phase; HbA1c, glycated hemoglobin; HDL, high-density lipoprotein; LV, left ventricular; MFAE, myocardial fatty acid esterification; MFAO, myocardial fatty acid oxidation; MFAU, myocardial fattu acid uptake; MMRGlu, myocardial metabolic glucose metabolism; M-value, whole body insulin sensitivity.</p>‡<p>adapted from Rijzewijk et al. 2009 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0059697#pone.0059697-Rijzewijk1" target="_blank">[23]</a>.</p

Expression and secretion of omentin-1 in intrathoracal adipose tissue depots.

<p>Representative Western blot (<b>A</b>) and quantification (<b>B</b>) of omentin-1 expression in paired epicardial (EAT), pericardial (PAT), and subcutaneous (SAT) adipose tissue biopsies of patients with (DM2, n = 7) and without (ND, n = 6) type 2 diabetes. Equal loading was verified by probing the immunoblots with glyceraldehyde 3-phosphate dehydrogenase (GAPDH) antibody. (<b>C</b>) Quantification of omentin-1 levels in conditioned media generated from paired EAT, PAT and SAT explants from DM2- and ND-patients. Data are expressed as mean ± SEM (n = 6 patients per group). ***indicates <i>P</i><0.001; **<i>P</i><0.01, *<i>P</i><0.05 for differences between ND and DM2 (ANOVA followed by Bonferonni analysis for multiple comparisons); ^###indicates <i>P</i><0.001; ^##<i>P</i><0.01, and ^#<i>P</i><0.05 for differences between the various fat depots (paired <i>t</i>-test).</p

Effect of recombinant omentin on sarcomere shortening and calcium fluxes in primary adult rat cardiomyocytes.

<p>Primary rat cardiomyocytes were incubated with control medium or conditioned media from epicardial adipose tissue from patients with type 2 diabetes (EAT) for 30 min in the absence or presence of recombinant omentin before analysis of sarcomere shortening and cytosolic Ca²⁺-fluxes. Effect of exposure of cardiomyocytes to EAT and omentin on departure velocity of contraction (<b>A</b>), peak sarcomere shortening (<b>B</b>), return velocity of contraction (<b>C</b>), departure velocity of cytosolic [Ca²⁺] (<b>D</b>), peak fura-2 fluorescence (<b>E</b>) and departure velocity of cytosolic [Ca²⁺] (<b>F</b>). Data were collected during at least 4 independent experiments using cardiomyocyte preparations from different rats and conditioned media from different donors, and are expressed as mean ± standard error of the mean. Differences among the groups were evaluated using the Kruskal-Wallis method followed by a Dunns multiple comparison test. ***<i>P</i><0.001; **<i>P</i><0.01, versus control adipocyte medium (control), ^###<i>P</i><0.001; ^##<i>P</i><0.01 EAT versus EAT+omentin.</p

Plasma omentin-1 levels in men with uncomplicated type 2 diabetes.

<p>Plasma omentin-1 levels, fat distribution, insulin sensitivity and diastolic parameters were determined in healthy control men (n = 14) and men with uncomplicated type 2 diabetes (DM2) (n = 78). (<b>A</b>) Whisker plot (median, min-max) depicting plasma omentin-1 levels in controls and DM2-patients. Differences in circulating omentin-1 levels were analyzed using a Mann-Whitney U-test. **indicates <i>P</i><0.01. Regression analysis identified significant correlations between baseline omentin-1 plasma levels and E peak filling rate (<b>B</b>), early deceleration peak (<b>C</b>), M-value (<b>D</b>), visceral fat volume (<b>E</b>), and systolic blood pressure (<b>F</b>). A straight line indicates a regression line for all subjects. A dashed line indicates a regression line for healthy controls only.</p

Characteristics of patients from which adipose tissue biopsies were collected.

<p>Data are presented as mean ± SD. <i>P</i>-values for differences between anthropometric variables were calculated using the Mann-Whitney U-test in case of continuous data, and using Fisher’s exact test for medication use.</p>*<p><i>P</i><0.05. BMI, body mass index; DM2, type 2 diabetes; ND, non-DM2.</p

Plasma omentin-1 levels in men with uncomplicated type 2 diabetes before and after 24-week pioglitazone treatment versus 24-week metformin treatment.

<p>(<b>A</b>) Plasma omentin levels before (0) and after 24 weeks of treating males with uncomplicated type 2 diabetes with metformin or pioglitazone. <i>P</i>-values for treatment-effects were calculated using a Wilcoxon signed rank test. **indicates a <i>P</i><0.01. Pearson regression analysis showed that only in the pioglitazone group changes in omentin-1 levels positively correlated with changes in early peak filling rate (<b>B</b>), early deceleration peak (<b>C</b>), and early deceleration mean (<b>D</b>).</p

Effect of recombinant omentin on insulin action in primary adult rat cardiomyocytes.

<p>Western blot (<b>A</b>) and quantification (<b>B</b>) of recombinant omentin on insulin action. Lysates from primary adult rat cardiomyocytes exposed for 24 h to control adipocyte medium (control) or recombinant omentin in the absence or presence of conditioned media generated from epicardial adipose tissue from patients with type 2 diabetes (EAT) were analyzed for insulin-induced Akt-Ser473-phosphorylation. Data were collected during at least 6 independent experiments using cardiomyocyte preparations from different rats and conditioned media from different donors, and are expressed as mean ± standard error of the mean. Open bars, basal; filled bars, insulin stimulated cells. Differences among the groups were evaluated by ANOVA following Bonferroni analysis for multiple comparisons. *<i>P</i><0.001 effect of insulin (filled bars) versus basal (open bars); ^###<i>P</i><0.001 control versus EAT, ^##<i>P</i><0.01 EAT versus EAT+omentin.</p