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. 2019 May 6;25:83–94. doi: 10.1016/j.molmet.2019.05.002

Figure 5.

Figure 5

ABHD15−/−mice showed no defects in glucose metabolism or insulin secretion. A-G, ABHD15−/− (KO) mice and wild type (WT) littermates were subjected to phenotypic characterisation. A, Mice were culled, tissues removed and subjected to immunoblotting with indicated antibodies, followed by quantification (scWAT, subcutaneous white adipose tissue; BAT, brown adipose tissue; n = 3, except BAT, islets: n = 2). B, Body weight (BW), lean mass (LM) and fat mass was determined (n = 16–17). C, Mice were subjected to glucose tolerance test (GTT) and area under the curve (AUC) was calculated (n = 10–13). D, Mice were subjected to insulin tolerance test (ITT) (n = 18–19). E, Blood glucose was measured under fed, 6-h fasted and overnight (ON) fasted conditions (n = 14–19). F, Blood insulin was measured at 0 and 15 min during the GTT (n = 11–13). G, Mice were culled, and pancreatic islets were isolated for assessment of glucose-stimulated insulin secretion (GSIS, n = 11–14). Data are mean ± SD (A) or mean ± SEM (B-G) with individual data points shown (except for ITT and GTT); * different from other conditions of the same genotype, *p < 0.05, ***p < 0.001, ****p < 0.0001; # different from WT, ##p < 0.01, ###p < 0.001, ####p < 0.0001; statistical significance was determined using two-tailed t-test (A-C) or two-way ANOVA with Tukey's or Sidak's multiple comparison test (E-G).