Fig. 1.

The metabolic phenotypes presented by Shp gene deletion are disrupted by cohousing scheme. A: BWs of WT and Shp^−/− mice fed WD from separate or cohousing scheme were measured and plotted with standard errors for the first 2-month regimen. (Separate WT, cohoused WT, cohoused Shp^−/−; n = 8. Separate Shp^−/−; n = 7). B: Hepatic TG concentrations (mg/g of liver weight) were quantified from the WT and Shp^−/− mice fed CD or WD in separate or cohoused cages for 6 months, and their averages were plotted with standard errors (n = 6). Two-way ANOVA and Student' t-test were performed to evaluate statistical significance. C: Livers from the experimental mice were processed for H&E staining. Representative H&E sections from mice fed WD were shown. White bars at right lower corner represent 100 μm length. D: Extracted lipids from livers of the WD-fed mice were analyzed using LC-MS. Average values of individual lipid class from each group (n = 4) were plotted in stacked columns. E: mRNA expression of hepatic genes responsible for inflammation were assessed using quantitative PCR analysis in cohoused WT and Shp^−/− mice and presented with average ± SEM (n = 4–6). #comparison with CD, ∗comparison with WT counterparts. Three symbols represent P < 0.005, two symbols P < 0.01, and one symbol P < 0.05. CE, cholesteryl ester; Cer, ceramide; CerPE, ceramide phosphatidylethanolamine; DAG, diacylglycerol; FFA, free fatty acid; HexCer, monohexylceramide; Hex2Cer, dihexylceramide; Hex3Cer, trihexosylceramide; IPC, inositolphosphorylceramide; MADAG, monoalkyldiacylglycerol; MIPC, mannosyl-inositol phosphorylceramide; M(IP)2C, mannosyl-di-(inositolphosphoryl) ceramide; PA, phosphatidic acid; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PG, phosphatidylglycerol; PI, phosphatidylinositol; PS, phosphatidylserine; SGalCer, 3-O-sulfogalatisylceramide; SM, sphingomyelin; TAG, triacylglycerol.