Mfsd2a KO mice have decreased liver TG with normal liver metabolism.

Abstract

<p>Oil red-O histology of fasted <i>A,</i> WT and <i>B,</i> KO liver illustrates neutral lipid stores. <i>C,</i> Quantification of TG extracted from fed and fasted WT and KO livers. <i>D,</i> Assay of β-oxidation in liver homogenates from fasted WT and KO littermates (n = 3–4 per genotype, data representative of three independent experiments). <i>E, In vivo</i> uptake of ¹⁴C-oleate in indicated tissues from WT and KO mice, normalized to heart uptake (n = 3 per genotype). <i>F,</i> TLC of lipid extract illustrating <i>in vitro</i> incorporation of ¹⁴C-glycerol and ¹⁴C-oleate by control and Mfsd2a-transfected HEK293 cells (n = 3). CE, cholesterol ester; M/D/TAG, mono-, di-, tri-acylglycerol; PL, phospholipids. <i>G-H, In vivo</i> VLDL production was assayed by measuring <i>G,</i> serum TG and H, cholesterol in fasted WT and KO mice (n>5 per genotype) following treatment with LPL-inhibitor F-127. <i>I,</i> Real-time PCR analysis of PPARα targets and fatty acid synthesis genes from fasted WT and KO liver (n = 3–4). <i>J</i>, Pyruvate tolerance test of 12–14-week old chow-fed WT and KO littermates after an overnight fast (n = 6). Data are displayed as mean ± SEM. * p<0.05, ** p<0.01.</p

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