The biochemical pathway for the production of androgens is discussed in Chapter 2. As in other steroidogenic cells, the cleavage of the side chain of cholesterol is confined to the mitochondria of the Leydig, or interstitial, cells of the testes. The role of the steroid acute regulatory protein, StAR, is the same in the Leydig cells as in other cells that carry out this side chain cleavage step, and as in other steroidogenic cells, this is the first and rate-limiting step in the production of testosterone.

Figure 1 summarizes the modifications of the steroid nucleus required to convert the 21-carbon result of cholesterol side chain cleavage, pregnenolone, to the 19-carbon androgens. The two main changes are the removal of carbons 20 and 21 and the oxidation of the 3β-hydroxyl group accompanied by migration of the double bond from the Δ5 to the Δ4 position. Depending on which of these two steps is carried out first, the pathway from pregnenolone to testosterone is called either Δ5 or Δ4, as outlined in Figure 1. The relative activities of the Δ5 and Δ4 pathway vary among various mammalian species; in the rodent the Δ4 pathway is predominant, while the human testis uses primarily the Δ5 pathway. All of these reactions occur in the microsomal fraction of the cell.

Fig1. Pathways of androgen synthesis. Androgens are synthesized in the Leydig cells of the testis by one of two pathways, depending on the species. In the Δ5 pathway from pregnenolone to testosterone (green), the cleavage of carbons 20 and 21 takes place before the oxidation of the 3β hydroxyl group and migration of the double bond from the Δ5 to the Δ4 position. In the Δ4 pathway (blue), the order of the two steps is reversed. The Δ5 pathway predominates in humans.

Figure 2 depicts the changes in testicular testosterone synthesis, as reflected in plasma hormone levels, throughout the life of a normal human male. The peak during the second trimester in utero is followed by another during the six months after birth. The relative quiescence of the androgen synthetic pathway persists throughout childhood until the beginning of the pubertal period. Plasma testosterone rises to adult levels by the end of puberty, and begins to decline in early middle age.

Fig2. Changes in human male plasma testosterone levels with age. During the second trimester of fetal development, levels of testosterone rise to nearly adult levels and a second peak is seen during the first half of the first year of postnatal life. Levels remain low during childhood until the pubertal rise to adult levels. This is followed by a decline with age for the remainder of life.

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مواضيع ذات صلة

Androgens and Related Molecules

Two-Dimensional Polyacrylamide Gel Electrophoresis

Isoelectric Focussing Gels

Native (Buffer) Gels

Sodium Dodecyl Sulfate (SDS)-Polyacrylamide Gel Electrophoresis

Transition Metals are Essential for Health

Individual Regulatory Events Combine to Form Sophisticated Control Networks

Regulation of Enzyme Quantity

Biochemical Evaluation of Cobalamin and Folate Deficiencies

Compartmentation Ensures Metabolic Efficiency & Simplifies Regulation

Regulation of Metabolite Flow can be Active or Passive

Catabolism of Catecholamines