Extended Data Fig. 2: Lpcat3AKO mice display no metabolic phenotype under standard laboratory conditions.
From: Dietary control of peripheral adipose storage capacity through membrane lipid remodelling
(a) Graphical illustration of in vivo Lpcat3AKO strategy. (b) qPCR analysis of Lpcat3 mRNA levels in fat depots and insulin target-tissues of 12-week-old NCD-fed control and Lpcat3AKO mice (n = 4, 4). (c) Lipidomic analysis of PC/PE or TG-FA species in the inguinal adipocyte fraction isolated from of 22-week-old NCD-fed control and Lpcat3AKO mice (n = 5, 5). (d) Body weight (BW) gain curves and composition of 22-week-old NCD-fed control and Lpcat3AKO mice (n = 30, 34). (e) Wet weights of the indicated tissues in NCD-fed control and Lpcat3AKO mice (n = 23, 25). (f) H&E stainings of iBAT and iWAT depots (scale bar, 100 µm). (g) qPCR analysis of iWAT of NCD-fed control and Lpcat3AKO mice (n = 7, 7). (h) 14C-oleate uptake in insulin-target tissues of 18-week-old NCD-fed control and Lpcat3AKO mice (n = 5, 7). Radioactivity (counts per min, CPM) was calculated in the extracted lipids from whole-organs 4 h post-gavage with 14C-Triolein and normalized for g/tissue. (i) Ex vivo lipolysis in dissected iWAT explants from 18-week-old NCD-fed control and Lpcat3AKO mice (n = 4, 4). Secreted glycerol was measured under basal and stimulated (2 µM isoproterenol, ISO) conditions. (j) Ex vivo β-oxidation in crude lysates prepared from iBAT, iWAT, and livers of 18-week-old NCD-fed control and Lpcat3AKO mice (n = 5, 5), assessed by conversion of 14C-palmitic acid to 14CO2. (k) Plasma TGs and cholesterol in 22-week-old NCD-fed control and Lpcat3AKO mice (n = 13, 7). Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 by Welch’s t-tests with Holm-Sidak’s correction on CLR-transformed values of each lipid class (c); or Welch’s t-tests with FDR correction using the Benjamini, Krieger, and Yekutieli procedure (b,g).
