Interaction between endocrine and paracrine peptides in prenatal growth control

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.

Maternal treatment with somatotropin during early gestation affects basic events of myogenesis in pigs

“…Nevertheless, it remains unclear whether higher nutrient availability affected cell proliferation directly or indirectly via hormones/growth factors controlled by nutrient intake (see Brameld et al 1998). Direct effects of increased growth hormone and IGF-I in maternal plasma (Kanitz et al 1995) on the embryos can be largely excluded, because there is no physiologically important transfer of peptide hormones across the placenta (Milner and Hill 1987;Fholenhag et al 1994).…”

Ontogeny of Insulin-Like Growth Factor-Binding Protein-1, −2, and −3: Quantitative Measurements by Radioimmunoassay in Human Fetal Serum

“…The American Pediatric Society and The Society for Pediatric Research announce the abstract deadline for the 1995 Annual Meeting (May [8][9][10][11]1995, San Diego Convention Center) has been set as January 3, 1995. For further information, contact: APSISPR Association Headquarters, 141 Northwest Point Blvd., P.O. Box 675, Elk Grove Village, IL 60009-0675, (708) 427-0205, Fax: (708) 427-1305.…”

Insulin-Like Growth Factor-I in the Parenterally Fed Low Birth Weight Infant

“…It is possible that because of morbidity and extreme pre maturity. the infants were unable to convert from a fetal synthetic pathway to a postnatal pattern; the concept of a primary hepatic source postnatally, however, is now disputed [3], Decreased somatomedin activity is seen in infants with intrauterine growth retarda tion [6]; the sick preterm infant with poor nutritional stores, and fed parenterally could be considered analogous to the growth-re tarded infant in utero. Assay cross-reactivity (4%) with IGF-II is unlikely to be signifi cant.…”

“…Growth of the fetus is rapid in the third trimester of pregnancy and is influenced by insulin-like growth factors [3]. The infant born significantly preterm has low energy and nitrogen reserves and is, because of added morbidity, at risk of significant clini cal undernutrition.…”