Fetal Endocrinology and Metabolism

Current Topics in Experimental Endocrinology, Vol. 5

L Martini, V. H. T. James

• Publisher: Academic Press
• Year: 2013
• Print ISBN: 9780121532055
• eBook ISBN: 9781483217376
• Topic: Medicine
• Subtopic: Physiology

Current Topics in Experimental Endocrinology, Volume 5: Fetal Endocrinology and Metabolism covers various aspects of fetal endocrinology. The book discusses studies of the hypothalamic-pituitary unit which emphasize the unique aspects of the fetal endocrine system; in vitro fertilization; and factors controlling placental endocrine function in domestic animals. The text also describes the role and kinetics of thyroid in fetal development; the placental transfer of carbohydrates; and fetal hormones and carbohydrate utilization. The regulation of partition of protein during pregnancy; the mineral needs of the fetus; and the fetal metabolism of cortisol are also considered. The book further tackles normal and abnormal sexual differentiation and the metabolic errors of adrenal steroidogenesis. Physiologists, endocrinologists, obstetricians, gynecologists, and students taking related courses will find the book invaluable.

Sexual Differentiation: Normal and Abnormal

Julianne Imperato-McGinley, DEPARTMENT OF MEDICINE, DIVISION OF ENDOCRINOLOGY, CORNELL UNIVERSITY MEDICAL COLLEGE, NEW YORK, NEW YORK

Publisher Summary

The undifferentiated gonad is formed from three sources—(1) coelomic epithelium, (2) underlying mesenchyme, and (3) primordial germ cells. The primordial germ cells develop into spermatogonia in the male and ova in the female; the sex cords become either seminiferous tubules or primary ovarian follicles; and the mesenchymal cells form either the Leydig cells or the theca and stromal cells in the female. Ovarian development from the undifferentiated gonad does not begin until approximately 50 days of gestation. The external genitalia, like the gonad, develop from common primordia: urogenital tubercle, urogenital swellings, and urogenital folds. Testicular differentiation occurs between the seventh and eighth week of intrauterine life. This chapter describes incomplete forms of androgen insensitivity. The known etiologic causes for male pseudohermaphroditism or incomplete masculinization can be divided into three basic categories—(1) the disorders of testicular differentiation and development, (2) the disorders of testicular function, and (3) the disorders of function at the androgen-dependent target areas.

I Embryology of Sexual Differentiation

A The Development of the Bipotential Gonad

B Gonadal Differentiation

C Phenotypic Differentiation

II Determinants of Phenotypic Differentiation

A Female Phenotypic Differentiation

B Male Phenotypic Differentiation

III Genetic Control of Sexual Differentiation

IV Sexual Differentiation of the Brain

V Male Pseudohermaphroditism

A Disorders of Testicular Differentiation and Development

B Disorders of Testicular Function

C Disorders of Function at Androgen-Dependent Target Areas

VI XX Males and True Hermaphroditism

A XX Males

B True Hermaphroditism

VII Female Pseudohermaphroditism

A Female Pseudohermaphroditism Secondary to Congenital Adrenogenital Hyperplasia (CAH)

B Virilization of the Female Fetus Secondary to Excess Maternal Androgen Production

References

I Embryology of Sexual Differentiation

A The Development of the Bipotential Gonad

An undifferentiated gonad is present in male and female fetuses and its development begins during the fifth week (5 to 14 mm) of fetal life. A thickened area of coelomic epithelium (germinal epithelium) appears on the medial aspect of the mesonephros and the proliferation of germinal epithelium cells and underlying mesenchyme produces a prominence on the medial side of the mesonephros known as the gonadal ridge. This is followed by proliferation of cords of cells (primary sex cords) from the epithelium into the mesenchyme. The gonad at this stage consists essentially of mesodermal cells of coelomic epithelial origin (Arey, 1965; Moore, 1973) (Fig. 1).

Fig. 1 Development of the biopotential gonad from the coelomic epthelium (primary sex cords), underlying mesenchymal tissue (medulla), and primordial germ cells and its differentiation to form a testes (adapted from Arey, 1965).

The primordial germ cells are visible early in the third week among the endodermal cells of the wall of the yolk sac near the origin of the allantois (Everett, 1943; Mintz and Russell, 1955, 1957). During folding of the embryo, part of the yolk sac is incorporated into the embryo and the primordial germ cells migrate along the dorsal mesentery to the gonadal ridges (Fig. 2). The germ cells are spherical and larger than the mesenchymal cells, with large vesicular nuclei and abundant cytoplasm. The germ cells multiply by mitosis during migration. In the fifth week of fetal life they begin to migrate into the underlying mesenchyme and by the end of the sixth week (13 to 15 mm) the undifferentiated or bipotential gonad is formed (Figs. 1 and 3).

Fig. 2 Migration of primordial germ cells from the endoderm of the yolk sac (Hamilton et al., 1972).

Fig. 3 Embryogenesis of the male phenotype.

Thus, the undifferentiated gonad is formed from three sources, coelomic epithelium, underlying mesenchyme, and primordial germ cells. The primordial germ cells develop into spermatogonia in the male and ova in the female; the sex cords become either seminiferous tubules or primary ovarian follicles; and the mesenchymal cells form either the Leydig cells or the theca and stromal cells in the female (Hamilton et al., 1972) (Figs. 1 and 4).

Fig. 4 The development of the bipotential gonad and its differentiation to form an ovary (adapted from Arey, 1965).

B Gonadal Differentiation

1 Testicular Differentiation

At approximately the seventh week of gestation in a 15- to 20-mm embryo, the testicular cords evolve from the primary sex cords of the indifferent gonad (Fig. 3). The Sertoli cells within each gonad enlarge, come into contact with one another, and engulf the germ cells. The distal ends of the testicular or seminiferous cords then interconnect to form a network of solid cords, the rete testes, which is in direct contact with the mesonephric tubules. At the third month of gestation the rete testes connect with the mesonephric tubules and by the sixth month the ends of the rete testes develop a lumen continuous with the mesonephric tubules which later develop into the ductuli efferen...

Table of contents

• Cover image
• Title page
• Table of Contents
• Contributors
• Editorial Board
• Copyright page
• Contributors
• Preface
• The Fetal Neuroendocrine Axis
• In Vitro Fertilization
• Factors Controlling Placental Endocrine Function in Domestic Animals
• The Fetal Thyroid
• Carbohydrate Metabolism
• Regulation of Partition of Protein During Pregnancy
• Mineral Needs of the Fetus
• Fetal Metabolism of Cortisol
• Sexual Differentiation: Normal and Abnormal
• Metabolic Errors of Adrenal Steroidogenesis
• Index