Figure 3
From: Phospholipase D1 deficiency in mice causes nonalcoholic fatty liver disease via an autophagy defect
The fat oxidation rate is reduced in the livers of Pld1−/− mice.
(a) Primary hepatocytes were isolated from Pld1+/+ and Pld1−/− littermates, serum starved, and treated with bovine serum albumin/palmitate complexes for 2 h. The oxygen consumption rate was measured at the indicated time points (n = 5 per each group). (b) The Pld1+/+ and Pld1−/− littermates were fed a HFD for 4 weeks starting at the age of 13 weeks (n = 9–11 per group) and qRT-PCR was performed. (c) The mice were maintained as described in (b) and the livers were collected. The mitochondria in the livers from Pld1+/+ and Pld1−/− littermates were visualized by transmission electron microscopy. The mitochondrial area was quantitatively measured using ImageJ (n = 3 mice per group). At least 15 pictures per group were evaluated. Scale bar, 0.2 μm. The data are presented as means ± SE or representative images from 3 to 5 independent experiments. *P < 0.05 versus the Pld1+/+ group. Abbreviations: HFD, high-fat diet; PA, palmitic acid; qRT-PCR, quantitative real-time polymerase chain reaction; SE, standard error.
