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Actions of FSH and LH on the testes
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FSH and LH influence spermatogenesis
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In the male, testosteroneView drug information biosynthesis occurs in the Leydig cells of the testes under the primary influence of LH (see Fig. 37.9). The LH receptor is a member of the G-protein coupled superfamily, which includes the receptors for TSH and FSH among many others (see Chapter 38). These receptors, with seven transmembrane spanning units, mediate the activation of adenylate cyclase, leading to regulation of the steroidogenic enzymes shown in Figure 37.7.
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Figure 37.9 Control of the hypothalamo-pituitary-gonadal axes. (A) In men, testosteroneView drug information is produced from cholesterol in the Leydig cell under LH stimulation. TestosteroneView drug information and FSH support spermatogenesis. (B) In women, estradiolView drug information (E2) is produced by the granulosa cell and the developing follicle after feedback stimulation. E2 feedback is mainly negative but, in midcycle, there is a positive E2 feedback resulting in the surge of LH that causes ovulation. ProgesteroneView drug information (P) is secreted by the resultant corpus luteum.
Among other functions, testosteroneView drug information facilitates the effects of FSH on spermatogenesis in the spermatic tubule. FSH binds to its specific receptor on the Sertoli cell of the testes and, by a mechanism similar to LH, induces increased synthesis of several proteins, including androgen-binding protein (ABP) and inhibin. ABP is secreted into the seminiferous tubular lumen where it binds testosteroneView drug information (or its active form dihydrotestosterone). This ensures a high local androgen concentration that, together with FSH, brings about the meiotic divisions that are necessary for spermatogenesis. Inhibin has a role in the FSH negative feedback loop (see Fig. 37.9).
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