Skip to main content
. 2019 Nov 8;31:55–66. doi: 10.1016/j.molmet.2019.10.007

Figure 4.

Figure 4

BAT-specific deletion of PEMT does not cause loss of UCP1. (A) Schematic of the targeting vector used to generate the PEMTcKO mice. (B) Genotyping PCR identifying the PEMT-BKO mice and loxP flanked controls. (C) PEMT mRNA levels in BAT, inguinal white adipose (iWAT), liver, and muscle, n = 3–4. (D) Body mass, n = 14–21. (E) Cold-tolerance test in the PEMT-BKO mice, n = 3. (F) Histology images of BAT stained with hematoxylin and eosin. (G) Protein levels of UCP1 and CS. (H) Protein levels of ETS complexes. (I) UCP1 and CS protein levels in adipose-specific PEMT knockouts (PEMT-AKO), liver-specific knockouts (PEMT-LKO), and skeletal muscle-specific knockouts (PEMT-MKO). (J) CL species in mitochondria isolated from BAT from the PEMT-BKO mice, n = 4–5. (K) PC species in isolated mitochondria from BAT from the PEMT-BKO mice, n = 4–5. Data are expressed as mean ± SEM, *p < 0.05.