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. 2010 Aug 10;5(8):e12057. doi: 10.1371/journal.pone.0012057

Figure 7. Effect of high-KAA diet on the production of hepatic and muscular lipotoxic metabolites.

Figure 7

Samples were obtained from C57B6 mice (n = 6 for each group) fed for 8 weeks with STD, HFD or the high KAA HFD (E/N = 1.8), except for (C) where mice were sampled at 2 weeks in addition to 8 weeks. Lipid species of free fatty acids (FFA), diacylglycerols (DAG) and ceramides (Cer) in the liver (A) and gastrocnemius muscle (B) were quantified using GC-MS, where c16 Cer, c18 Cer, c20 Cer and c22 Cer correspond to palmitoyl-ceramide, stearoyl-ceramide, arachidyl-ceramide and docosanoyl-ceramide, respectively. Changes in liver c16 Cer and muscle c18 Cer concentrations were tracked between 2- and 8-week feeding periods (C). Metabolic pathway fluxes of hepatic and muscular ceramides were assessed by quantifying the contributions from palmitoyl-CoA (f1, f2) and stearoyl-CoA (f3) (see D left). The contribution of DNL-derived FA to ceramide synthesis was evaluated based on deuterium labeling of sphingosine- and acyl-groups (D), whereas non-DNL derived FA is illustrated with a blue column on the bottom of each bar. All values are expressed as mean+/−SEM (n = 6). *: p<0.05 for all high-fat groups as compared to STD group; #: p<0.05 for the high-KAA group as compared to HFD control.