Abstract
To evaluate the intrauterine growth restriction (IUGR) by the expression of IR-β, IRS-1, IRS-2, IGF-IRβ and Ikappaβ in experimental model of gastroschisis. Pregnant rats at 18.5 days of gestation were submitted to surgery to create experimental fetal gastroschisis (term = 22 days) were divided in three groups: gastroschisis (G), control (C) and sham (S). Fetuses were evaluated for body weight (BW), intestinal (IW), liver (LW) and their relations IW/BW and LW/BW. IR-β and IGF-IRβ receptors, IRS-1 and IRS-2 substrates and Ikappaβ protein were analyzed by western blotting. BW was lower in G, the IW and IW / BW were greater than C and S (p<0.05) groups. The liver showed no differences between groups. In fetuses with gastroschisis, compared with control fetuses, the expression of IGF-IRβ (p<0.001) and Ikappaβ (p<0.001) increased in the liver and intestine, as well as IR-β (p<0.001) which decreased in both. In contrast to the intestine, IRS-1 (p<0.001) increased in the liver and IRS-2 decreased (p<0.01). The axis of the intestine liver has an important role in inflammation, with consequent changes in the metabolic pathway of glucose can contribute to the IUGR in fetuses with gastroschisis.
Highlights
Gastroschisis is a congenital defect characterized by an opening on the abdominal wall, usually right to the umbilical cord, which affects five in 10,000 live births[1]
We observed a significantly lower body weight and increased intestinal weight and IW/BW ratio in fetuses with gastroschisis compared with controls and shams (p
Intestinal expression of IR substrates (IRS)-2 was higher in G and C groups compared with S group, but it was not statistically different
Summary
Gastroschisis is a congenital defect characterized by an opening on the abdominal wall, usually right to the umbilical cord, which affects five in 10,000 live births[1]. A proper intestinal length is required for fetal somatic growth. Intestinal anomalies such as gastroschisis may cause intrauterine growth restriction (IUGR) with birth weight less than expected for gestational age[3,4]. The causes of IUGR in gastroschisis are still not known, it might be due to the defect itself or to secondary causes like the metabolic response of the bowel in contact with the amniotic fluid[5]. In the rat model of gastroschisis the body weight is decreased and there is an inverse relationship between the length of exposure of the bowel to the amniotic fluid and body weight, so that longer exposure leads to a more decreased body weight in fetuses with gastroschisis[6]
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