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. 2019 Nov 21;39(1):e100882. doi: 10.15252/embj.2018100882

Figure 6. Prenatal psychostimulant exposure impairs glucose homeostasis in adult offspring.

Figure 6

  • A, B
    Immunohistochemistry for insulin and glucagon in pancreatic islets of 6‐week‐old offspring born to drug‐exposed mothers (A). Sex assignment shows that females respond to prenatal drug exposure with permanently reduced insulin levels. (A1) Representative images from females are shown and were counterstained with Hoechst 33342 (pseudo‐colored in gray). Scale bar = 40 μm. (B) Ins2 mRNA expression remains reduced in adult offspring exposed in utero to psychostimulants (pooled data). Quantitative data in (A, B) are from n ≥ 3 mice/group and were expressed as means ± SD.
  • C, D
    Blood glucose profiles during glucose tolerance test in females (C) and males (D) at 6 weeks of age.
  • E, F
    Quantification of the “area under the curve” (AUC) indicates glucose intolerance in female mice prenatally exposed to psychostimulants with only amphetamine‐treated males showing significantly increased AUC.
  • G
    Insulin immunoreactivity no longer differed between amphetamine‐exposed and control mice, irrespective of their sex, at 1 year of age. (G1) Representative images; Scale bar = 65 μm.
  • H
    The bodyweight of 1‐year‐old female mice prenatally exposed to amphetamine was significantly reduced versus vehicle‐treated controls.
  • I, J
    Blood glucose profiles during glucose tolerance testing in females (I) and males (J) at 1 year of age.
  • K
    AUC indicates glucose intolerance in female but not male mice prenatally exposed to amphetamine.
Data information: Quantitative data were normalized to those in control and expressed as means ± SD (for visual clarity SD were omitted in C, D, I, J); n ≥ 3 animals/group/sex were analyzed (from 3 to 4 pregnancies each). ***P < 0.001, **P < 0.01, *P < 0.05 (pair‐wise comparisons after one‐way ANOVA).