By J.-C. Carel, Paul A. Kelly

In mammals, the main elements excited by the law of physique development are recognized: insulin-like progress elements (IGF) are key regulators of somatic development. development hormone (GH), secreted via the pituitary gland, without delay regulates circulating degrees of IGF-I, that is the foremost coordinator of spatio-temporal development of the organism. In people, progress is much more complicated, regarding a few particular features no longer present in different species. those comprise quick intrauterine progress, deceleration simply after start, a mid-childhood development spurt, a moment deceleration prior to puberty, a teenager development spurt, and at last complete statural development, that's visible slightly later. The mixed wisdom about the endocrine and paracrine elements of development have resulted in the advent of therapy regimens, superior in GH-deficient young ones. even if, dimension will depend on the mix of a couple of genetic components, and there stay a number of elements of this complicated technique nonetheless poorly understood.

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Maternal under-nutrition and disease are less common determinants of birth weight in contemporary populations (Mathews et al. 1999). Maternal hypertension and pre-eclampsia are associated with impaired placental function and reduced birth weight, whereas maternal diabetes often results in fetal macrosomia. Thus, size at birth is a complex trait that reflects both the maternal-uterine environment and fetal genes. Genetic Control of Size at Birth 29 Maternal uterine environment Size at birth is the most important determinant of perinatal survival (Karn and Penrose 1951), yet, in most populations, mean birth weight is slightly lower than that which is optimal for offspring survival (Alberman 1991).

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2003). Infants with a reduced or increased copy number of the type 1 IGF receptor were also reported to show reduced and increased fetal and postnatal growth, respectively (Okubo et al. 2003), indicating that the copy number of IGF1R may influence growth in humans. Subjects with the fetal overgrowth Beckwith Wiedemann syndrome had over-expression of IGF-2 in association with genetic defects in the IGF2 gene (Morison et al. 1996). As yet, there have been no reported human cases with severe mutations of the IGF2R gene, but variable expression of this gene has been reported in relation to size at birth (Wutz et al.

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Deciphering Growth by J.-C. Carel, Paul A. Kelly
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