Sexual differentiation in humans development can only occur when the fetal testis secretes key hormones at a critical period in early gestation. The testes begin to secrete three hormones that influence the male internal and external genitalia: they secrete anti-müllerian hormone (AMH), testosterone, and dihydrotestosterone (DHT). Anti-müllerian hormone causes the paramesonephric ducts to regress. Testosterone converts the mesonephric ducts into male accessory structures, including the epididymis, vas deferens, and seminal vesicle. Testosterone will also control the descending of the testes from the abdomen into the scrotum. Many other genes found on other autosomes, including"WT-1", "SOX9", "SF-1" also play a role in gonadal development. Females:
Adrenocortical hormone and increased blood potassium levels caused by a deficiency of aldosterone. These electrolyte imbalances induce nerve and muscle issues. Other symptoms include fatigue, salt cravings, weight loss, and increased skin pigmentation. Increased skin pigmentation is caused by a deficiency of the adrenocortical hormone hydrocortisone. Its normal behavior would be as negative feedback at the pituitary gland, stimulating the pituitary gland to decrease secretion of corticotropin. Because hydrocortisone is not able to be produced in Addison’s disease, the pituitary gland continues to secrete corticotropin which binds to the receptor for melanocyte-stimulating hormone. It then causes melanocytes to produce more pigment, thus