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. Author manuscript; available in PMC: 2012 Aug 17.
Published in final edited form as: Diabetologia. 2011 Aug 17;54(11):2931–2940. doi: 10.1007/s00125-011-2272-8

Fig. 1.

Fig. 1

Indices of lipid peroxidation in LDL from control volunteers, obese patients with MetS or type 2 diabetes: fatty dimethylacetals (DMA) derived from PE plasmalogens (a), 9- and 13-HODE (b), HODE/18:2n-6 ratio (c) and MDA (d). Data are means ± SEM (n= 7 to 10 subjects per group). LDL from MetS patients vs LDL from control volunteers : significantly different (p < 0.05) for 16:0 DMA, 18:0 DMA, DMA sum, 9-HODE, 13-HODE, HODE/18:2 n-6 and (p < 0.01) for MDA. LDL from type 2 diabetic patients vs LDL from control volunteers : significantly different (p < 0.01) for 16:0 DMA, 18:0 DMA, 18:1 n-9 DMA, DMA sum and MDA ; significantly different (p < 0.05) for 9-HODE, 13-HODE and HODE/18:2 n-6. LDL from type 2 diabetic patients vs LDL from MetS patients : significantly different (p < 0.05) for 16:0 DMA, 18:0 DMA, 18:1 n-9 DMA and DMA sum. p values were obtained by ANOVA followed by Fisher’s PLSD post hoc test. HODE, hydroxy-octadecadienoic acid; MDA, malondialdehyde; DMA, dimethylacetals; PE, phosphatidylethanolamine.