Glucokinase and IRS-2 are required for compensatory β cell hyperplasia in response to high-fat diet–induced insulin resistance
J. Clin. Invest. Yasuo Terauchi, et al. 117:246 doi:10.1172/JCI17645 [
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Figure 4Changes in gene expression levels in the islets of
Gck+/– mice on the HF diet.
(
A) RT-PCR analysis of
Irs1,
Irs2,
Igf1r,
Prlr,
Ipf1, and
Arbp (36B4), shown as a control. Islets were isolated from wild-type or
Gck+/– mice after 20 weeks on standard chow or HF diet. Experiments were replicated at least 3 times, and typical images are shown. (
B) Western blot analysis of
Irs2,
Igf1r,
Insr,
Ipf1, and
Akt1. Islets were isolated from wild-type or
Gck+/– mice after 20 weeks on standard chow or HF diet,
Irs1–/– mice, and
Irs2–/– mice on standard chow (
n = 3). Equal amounts of lysates (20 μg) were blotted with the antibody indicated. Quantitative determination of the β cell mass of islets less than 250 μm in diameter revealed the values in the 4 mouse groups to be indistinguishable (standard chow–fed wild-type, 0.81% ± 0.03%; HF diet–fed wild-type, 0.85% ± 0.03%; standard chow–fed
Gck+/–, 0.82% ± 0.02%; HF diet–fed
Gck+/–, 0.84% ± 0.02%). (
C) Each expression level was quantified (
n = 4–6). *
P < 0.05; **
P < 0.01.
