Figure 1.
Expression and secretion of omentin-1 in intrathoracal adipose tissue depots.
Representative Western blot (A) and quantification (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. (C) 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 P<0.001; **P<0.01, *P<0.05 for differences between ND and DM2 (ANOVA followed by Bonferonni analysis for multiple comparisons); ###indicates P<0.001; ##P<0.01, and #P<0.05 for differences between the various fat depots (paired t-test).
Table 1.
Characteristics of patients from which adipose tissue biopsies were collected.
Figure 2.
Plasma omentin-1 levels in men with uncomplicated type 2 diabetes.
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). (A) 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 P<0.01. Regression analysis identified significant correlations between baseline omentin-1 plasma levels and E peak filling rate (B), early deceleration peak (C), M-value (D), visceral fat volume (E), and systolic blood pressure (F). A straight line indicates a regression line for all subjects. A dashed line indicates a regression line for healthy controls only.
Table 2.
Characteristics of subjects for determination of circulating omentin-1 levels.
Table 3.
Correlations between plasma omentin-1 levels and anthropometric, plasma, hemodynamic parameters, and cardiac dimensions and function.
Figure 3.
Plasma omentin-1 levels in men with uncomplicated type 2 diabetes before and after 24-week pioglitazone treatment versus 24-week metformin treatment.
(A) Plasma omentin levels before (0) and after 24 weeks of treating males with uncomplicated type 2 diabetes with metformin or pioglitazone. P-values for treatment-effects were calculated using a Wilcoxon signed rank test. **indicates a P<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), early deceleration peak (C), and early deceleration mean (D).
Figure 4.
Effect of recombinant omentin on sarcomere shortening and calcium fluxes in primary adult rat cardiomyocytes.
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 (A), peak sarcomere shortening (B), return velocity of contraction (C), departure velocity of cytosolic [Ca2+] (D), peak fura-2 fluorescence (E) and departure velocity of cytosolic [Ca2+] (F). 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. ***P<0.001; **P<0.01, versus control adipocyte medium (control), ###P<0.001; ##P<0.01 EAT versus EAT+omentin.
Figure 5.
Effect of recombinant omentin on insulin action in primary adult rat cardiomyocytes.
Western blot (A) and quantification (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. *P<0.001 effect of insulin (filled bars) versus basal (open bars); ###P<0.001 control versus EAT, ##P<0.01 EAT versus EAT+omentin.