Fig. 1
Glucose disposal after acute apoA-I treatment. (
a) Schematic description of animal treatment and analysis. Mice were analysed for serum insulin (s-insulin) and glucose (s-glucose) after apoA-I injection (this figure) or, in separate groups of mice, for their glucose-disposal capacity in a GTT performed 3 h after apoA-I injection (see Fig.
2). HFD-fed mice exhibited elevated basal fasting glucose (
b) and insulin (
c) compared with ND-fed mice. (
d) Serum samples collected 3 h after injection were separated (2 μl) under native conditions, and the administered human apoA-I was detected using immunoblotting; 0.15 μg purified lipid-free (LF) apoA-I and 0.15 μg synthesised lipid-bound (LB) apoA-I in discoidal HDL particles were used as controls. Arrows indicate migration distance of HDL (top) and lipid-free apoA-I (bottom). Serum glucose (
e,
f) and insulin (
g,
h) levels at 0, 1, 2 and 3 h after a single injection (14 mg/kg body weight) of apoA-I WT (white triangles/dash-dot line in [
e,
g]; black triangles/dash-dot line in [
f,
h]), apoA-I Milano (white upside down triangles/solid line in [
e,
g]; black upside down triangles/solid line in [
f,
h]) or NaCl (black circles/dashed line in [
e,
g]; black squares/dotted line in [
f,
h]) in fasted ND (
e,
g) or HFD (
f,
h) animals are shown. (
b,
c)
n = 29; ****
p < 0.0001, HFD mice vs ND mice using non-parametric Mann–Whitney test. (
e–
h)
n = 6–8; ***
p < 0.001 for apoA-I (WT or Milano) vs NaCl HFD control using two-way ANOVA with Bonferroni’s post hoc test