The testes produce several hormones, with testosterone being the most abundant and well known. But they also secrete inhibin B, anti-Müllerian hormone (AMH), insulin-like factor 3 (INSL3), and small amounts of estrogen. Each comes from a specific cell type within the testes and plays a distinct role in male development, fertility, and overall health.
Testosterone: The Primary Testicular Hormone
Testosterone is produced by Leydig cells, which sit in the tissue between the sperm-producing tubes of the testes. The process starts when the brain’s pituitary gland releases luteinizing hormone (LH) into the bloodstream. LH binds to receptors on Leydig cells and triggers them to convert cholesterol into testosterone through a series of enzymatic steps inside the cell.
In healthy adult males aged 19 and older, total testosterone typically falls between 300 and 1,000 ng/dL. Levels fluctuate throughout the day, peaking in the morning and dipping in the evening. During puberty, testosterone drives the deepening of the voice, growth of facial and body hair, increase in muscle mass, and maturation of the reproductive organs. In adulthood, it continues to maintain muscle and bone density, regulate fat distribution, support red blood cell production, and fuel sex drive and sperm production.
Testosterone also acts as a chemical signal back to the brain. When levels rise high enough, the hypothalamus and pituitary gland reduce their output of the hormones that stimulate the testes. This negative feedback loop keeps testosterone within a functional range without conscious effort.
Inhibin B: The Fertility Signal
Sertoli cells, which line the inside of the sperm-producing tubes, secrete inhibin B. This hormone’s primary job is regulating sperm production by communicating with the pituitary gland. When Sertoli cells release inhibin B into the bloodstream, it suppresses the pituitary’s release of follicle-stimulating hormone (FSH). Less FSH means less stimulation of sperm production, so inhibin B essentially acts as a brake that prevents overproduction.
Clinically, inhibin B levels serve as a useful window into how well the testes are making sperm. Research has found a significant positive correlation between inhibin B levels and sperm concentration. In one study, when inhibin B dropped below 80 pg/mL and FSH climbed above 10 IU/L, the predictive power for detecting low sperm counts was 100%. This makes inhibin B one of the more direct blood markers of sperm-producing capacity, which is why fertility specialists sometimes measure it alongside standard hormone panels.
Anti-Müllerian Hormone (AMH)
AMH is best known for its role very early in life. During fetal development, around weeks 7 to 8 of gestation, Sertoli cells begin producing AMH. Its critical job at this stage is triggering the breakdown of the Müllerian ducts, the structures that would otherwise develop into a uterus and fallopian tubes. Without AMH, these structures persist regardless of genetic sex. Mutations affecting either the AMH gene or its receptor can lead to a condition where male individuals retain uterine tissue alongside otherwise normal male anatomy.
What surprises many people is that AMH production doesn’t stop after fetal development. The testes continue secreting it through childhood and into adulthood, though levels gradually decline with age. Its exact function in adult males is less clearly defined than its fetal role, but it remains a measurable marker of Sertoli cell activity.
Insulin-Like Factor 3 (INSL3)
INSL3 is a less well-known hormone produced by Leydig cells alongside testosterone. Its most important role occurs during fetal development, when it drives the descent of the testes from the abdomen into the scrotum. This process normally happens before birth. Mutations in the INSL3 gene or its receptor can cause cryptorchidism, the condition where one or both testes fail to descend properly.
In adults, INSL3 continues to circulate in the blood and is considered a marker of mature Leydig cell function. Receptors for INSL3 have been found in several tissues beyond the reproductive system, suggesting it may play roles in adult health that researchers are still working to define. Because INSL3 production depends on having a healthy population of mature Leydig cells, low levels can signal problems with testicular function even when testosterone levels still appear normal.
Small Amounts of Estrogen
The testes also produce estradiol, the most potent form of estrogen. This happens through a process called aromatization, where an enzyme converts some testosterone into estradiol directly within testicular tissue. The amounts are small compared to testosterone, but they’re physiologically important. Estrogen in males helps regulate bone density, fat metabolism, and even aspects of sperm maturation. The balance between testosterone and estrogen matters more than the absolute level of either one alone.
How the Brain Controls It All
None of these hormones operate independently. They’re coordinated through a feedback system connecting the hypothalamus, the pituitary gland, and the testes. The hypothalamus releases gonadotropin-releasing hormone (GnRH), which tells the pituitary to secrete LH and FSH. LH stimulates Leydig cells to produce testosterone and INSL3. FSH stimulates Sertoli cells to support sperm production and secrete inhibin B.
The feedback works in both directions. Rising testosterone levels suppress GnRH and LH production, slowing further testosterone synthesis. Rising inhibin B levels suppress FSH, reducing stimulation of the Sertoli cells. This creates a self-correcting system that keeps hormone levels and sperm production in a functional range. When any part of this loop is disrupted, whether by aging, injury, medication, or disease, the downstream effects can show up as low testosterone, reduced fertility, or both.
Two Waves of Hormone Production
The testes don’t produce hormones at a constant rate across a lifetime. There are two distinct peaks driven by two separate populations of Leydig cells. The first wave comes from fetal Leydig cells, which produce the high testosterone levels needed to masculinize the developing reproductive tract and brain. These cells decline after birth, and testosterone drops to very low levels during early childhood.
The second wave begins at puberty, when a new population of adult Leydig cells develops from stem cells within the testes. These cells ramp up testosterone production to the adult range of 300 to 1,000 ng/dL, driving the physical changes of puberty. This adult population then sustains hormone production for decades, though output gradually declines with aging. The gap between these two waves explains why prepubertal boys have very low testosterone despite having testes that were hormonally active before birth.