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Interaction between endocrine and paracrine peptides in prenatal growth control
Insights
Fetal growth relies on insulin and placental lactogen (PL), not pituitary hormones. Optimal fetal development requires a balance of hormones, tissue growth factors, and nutrition.
Area of Science:
- Endocrinology
- Developmental Biology
- Reproductive Medicine
Background:
- Fetal growth regulation differs significantly from postnatal growth.
- The roles of pituitary hormones in fetal development are minimal.
- Understanding fetal endocrinology is crucial for addressing growth abnormalities.
Purpose of the Study:
- To review the endocrine mechanisms governing fetal growth.
- To elucidate the specific roles of hormones and growth factors in prenatal development.
- To establish a framework for understanding fetal growth regulation.
Main Methods:
- Review of existing scientific literature on fetal endocrinology.
- Analysis of hormonal and tissue factor involvement in fetal growth.
- Integration of nutritional influences on prenatal development.
Main Results:
- Insulin is vital for fetal anabolism, acting permissively to regulate growth rate.
- Placental lactogen (PL) and related peptides may function as primary fetal growth hormones.
- Growth hormone (GH) has an ill-defined role in fetal pancreatic development and insulin secretion.
- Local tissue growth factors, like somatomedins, are critical and interact with nutrition.
Conclusions:
- Fetal growth is regulated by a complex interplay of hormones (insulin, PL), tissue growth factors, and maternal nutrition.
- A hierarchical model is insufficient; these factors interact dynamically.
- Further research is needed to fully define the ontogeny of fetal endocrine systems and their interaction with growth factors.
Abstract:
The evidence reviewed here shows that the endocrinology of fetal growth is very different from that operating postnatally. Pituitary hormones play little part in stimulating growth of the lean body mass or skeleton although growth hormone (GH) may be involved, in some as yet ill defined way in the ontogeny of the fetal pancreatic islet and insulin secretion. Insulin is important because it stimulates fetal cellular anabolism but acts in a permissive manner: with too little insulin growth is inhibited, with too much growth proceeds at a genetically predetermined rate. Placental lactogen (PL), or other peptides within the GH/PL family, may act as a true growth-promoting hormone in the fetus; it stimulates both cellular metabolism and mitosis. The part played by endocrine control mechanisms in the fetus is set in context by an appreciation of the importance of locally acting tissue growth factors, and in particular the somatomedins. Their part in fetal growth control is intimately bound up with the plane of nutrition experienced by the fetus. It is concluded that the simplest analysis that makes biological sense involves a consideration of hormones, tissue growth factors and nutrition, not hierarchically but as mutually interacting variables.