Levels of testosterone estrogen and progesterone

Testosterone is formed from its precursor androstenedione and to a lesser extent from DHEA. In males, testosterone is produced mainly by Leydig cells of the testes. Testosterone can be converted by peripheral tissues to the more active dihydrotestosterone (DHT) by the enzyme 5a-reductase or it can be converted into estradiol (E2) by an "A" ring aromatase. In males, the conversion of testosterone to E2 by aromatase achieves masculinization of brain neurons (Wu et al. 2009). In the female ovary, testosterone secreted by thecal cells of the follicles is aromatized by granulosa cells into estradiol.

In males testosterone levels reach «250 ng/L by the second trimester of gestation. 2-3 months after birth, the levels fall to 50ng/L and remain low until puberty (age 12-17), when they rise to adult levels of 500-750ng/L. Levels of testosterone decline slowly after middle age, but inadequate testosterone levels can be augmented by hormone replacement therapy

(Wilson et al. 1998). In females, testosterone levels are normally low: 30-50 ng/L throughout life (Forest 1975). Serum testosterone is converted into inactive metabolites by the liver.

Levels of E2 are low in girls (1.6-2.6 pg/ mL) but even lower in boys (0.4 to 1.1 pg/ mL (Janfaza et al. 2006). During puberty (age 8-13) estrogen rises to adult levels and varies during the menstrual cycle. Estradiol shows a pre-ovulatory peak (190pg/ml) by day 14 of the cycle and peaks broadly («100pg/ mL) during the luteal phase from days 18-25 (Levin and Hammes 2011; Thorneycroft et al. 1971). Progesterone is low except for a broad peak at 10 ng/ mL during the luteal phase of the menstrual cycle. After menopause, E2 falls, reaching levels similar to those found in adult males (8-40 pg/mL) (Lee et al. 2006). Estrogen replacement can be used to ameliorate the side effects of low estradiol. Contraception employs small doses of an ethinylestradiol and progesterone, but studies have shown no relationship between current and past use of contraceptives and diabetic retinopathy (Klein et al. 1990).

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