Effects of food restriction and pregnancy on the expression of insulin-like growth factors-I and -II in tIssues from guinea pigs

Abstract

The insulin-like growth factor (IGF) system is subjected to pregnancy-associated changes in the circulation and is suggested to be of importance for partitioning of nutrients between the mother and the foetus. Interestingly, maternal undernutrition alters the pregnancy-associated changes, with possible adverse consequences for the mother and the foetus. However, it is not known how malnutrition and pregnancy alter the expression of mRNA for IGFs locally in different tissues. The aims of this study were to investigate where IGF-I and IGF-II are expressed in guinea pigs and how this expression is altered during food restriction and pregnancy. Ad libitum-fed and foodrestricted (fed 70% of the ad libitum-fed intake four weeks before pregnancy and throughout the study) guinea pigs were mated. On day 40 of pregnancy and on the corresponding day for virginal females the animals were killed. mRNA for IGF-I and IGF-II was analysed in various organs/tissues by solution hybridisation. mRNA for IGF-I was expressed in high amounts in uterus, liver and adipose tissues. The expression was not affected by food restriction, but was increased in liver and adipose tissue and decreased in uterus by pregnancy. mRNA for IGF-II was expressed in high amounts in the placenta and liver. In the placenta the expression was decreased by food restriction. Pregnancy increased the levels of mRNA for IGF-II in the liver. Food-restricted dams had smaller foetuses and placentas. In conclusion, this study indicates an important role for the adipose tissue during gestation, not only as an energy store but also as an endocrine tissue expressing IGF-I. The decreased expression of IGF-II in the placenta due to food restriction is suggested to have adverse effects on placental structure and function.

Late pregnancy increases hepatic expression of insulin-like growth factor-I in well nourished guinea pigs

“…Hepatic IGF-I mRNA as measured by quantitative RT-PCR ELISA late in pregnancy was fourfold higher than in the non-pregnant state, in the ad libitum fed guinea pig. However, IGF-I expression in liver of pregnant guinea pigs analyzed by solution hybridization and an RNase protection assay, a method which differs from that used in the current study, also appears to be about twice as high as in mid-gestation, when referenced to that in non-pregnant ad libitum fed guinea pigs studied concomitantly [14]. This contrasts with other species, such as the rat [10,[15][16][17][18] and cow [19], where hepatic abundance of IGF-I mRNA increases in early gestation, then decreases in late gestation and is no longer elevated compared to the non-pregnant state.…”

Effects of restricted feeding on fetal and placental development in pregnant rabbits

“…In the histological examination of the placenta, the labyrinth zone was signifi cantly thinner and the basal zone was signifi cantly thicker in the RF group than in the NT group. An abnormally thin labyrinth zone is a common fi nding of intrauterine growth retardation in rats (Yokoi et al, 2008) and rabbits (Zhang et al, 1995), and a decreased placental surface area with decreased numbers of end villi is said to be related to decreased transport of nutrition to the fetus, resulting in fetal growth inhibition (Constância et al, 2002, Zygmunt et al, 2003Olausson et al, 2003). It is known that in the placenta of rabbits, PAS-positive glycogen-containing cells in the basal zone almost disappear during the late gestational period.…”

Programming of obesity and cardiovascular disease

“…Calorie restriction has been found to either decrease or not IGF levels at birth and to increase or not IGF binding proteins (IGFBPs). 55,56 Protein restriction decreased plasma IGF-1 levels in the progeny at birth, 57,58 as well as augmented the abundance of IGFBP-1 and -2, the liver production of which being regulated in part by insulin and glucocorticoids. 58 A third pathway of generating obesity in children and adult is a modification in the population of fat cell precursors.…”