Table 1 Insulin signalling-associated gene expression and pathway activation are not altered in adolescent female offspring exposed to excess androgen during fetal life.

From: Developmental programming of polycystic ovary syndrome (PCOS): prenatal androgens establish pancreatic islet α/β cell ratio and subsequent insulin secretion

End point

Female control

Female TP

Significance

Western blot

 Hepatic tERK: pERK

6.88 ± 2.50

8.87 ± 3.74

NS

 SM tERK: pERK

1.01 ± 0.49

1.47 ± 0.87

NS

 Hepatic tAKT: pAKT

0.58 ± 0.16

0.75 ± 0.33

NS

 SM tAKT: pAKT

0.52 ± 0.32

0.66 ± 0.07

NS

qRT-PCR

 Hepatic SLC2A1

2.93 ± 1.02

4.99 ± 1.44

NS

 SM SLC2A1

0.97 ± 0.29

0.82 ± 0.12

NS

 Hepatic SLC2A4

2.61 ± 0.62

3.98 ± 0.92

NS

 SM SLC2A4

0.93 ± 0.2

1.18 ± 0.16

NS

 Hepatic IRS1

4.1 ± 1.43

5.87 ± 1.73

NS

 SM IRS1

0.40 ± 0.19

2.28 ± 0.69

NS

 Hepatic INSR

3.09 ± 0.99

4.58 ± 1.47

NS

 SM INSR

1.02 ± 0.17

0.61 ± 0.09

NS

  1. Insulin signalling genes and phosphorylation of ERK1/2 and AKT were quantified in a random subset of 11 month old female offspring from control (n = 5) and TP treated pregnancies (n = 5), in skeletal muscle (SM) and hepatic tissue samples obtained at sacrifice, 15 minutes post intravenous glucose bolus administration. There was no significant (NS) effect of TP treatment upon any of the end-points quantified. Data represents mean ± s.e.m.
Back to article page