Abstract
The maternal environment affects fetal development and may influence the physiology of the adult. Fetal growth hormone (GH) is increased by maternal undernutrition but the mechanisms responsible are unknown. This study determined the effect of maternal undernutrition on the development of fetal pituitary somatotropes in the female. Ewes were grouped randomly into control (fed 100% of requirements) or nutrient restricted (fed 50%) from Days 28 to 78 of gestation. At Day 78, the ewes were killed and fetuses collected (Day 78 NR (nutrient restricted): n = 6; Day 78 C (control): n = 6). Remaining ewes were realimented to 100% of nutritional requirements and were killed at Day 135 (Day 135 NR (nutrient restricted): n = 6; Day 135 C (control): n = 6). Somatotropes were visualized immunocytochemically and the size, mean density, total percentage and proportion colocalized with substance P were determined for each group. Nutrient restriction increased ( p < 0.01) the density of pituitary cells in Day 78 fetuses but this difference was no longer apparent by Day 135 after realimentation. The density and proportion of somatotropes were not different between treatment groups at Day 78 but were significantly ( p < 0.05) lower in the nutrient restricted Day 135 fetuses as compared to the Day 135 control animals. Somatotropes from restricted fetuses were significantly ( p < 0.001) larger at Day 78. Nutrient restriction increased the density ( p < 0.001) and percentage ( p < 0.05) of substance P-immunoreactive cells Day 135 fetuses. Similarly, the proportion of somatotropes that expressed substance P was significantly ( p < 0.05) increased by nutrient restriction in the Day 135 fetuses. Although nearly two thirds of substance P-immunoreactive cells co-expressed GH, there was no significant effect of treatment on this co-expression. Additional studies are required to determine if other components of the neuroendocrine GH axis are affected by this nutritional insult, if the alterations that we have observed, particularly in the tachykinin system, persist into adulthood and, importantly, what are the long-term consequences of an altered GH axis.
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