The pancreas secretes the hormones insulin, glucagon, and somatostatin, also known as growth hormone inhibiting hormone (GHIH). Insulin and glucagon have reciprocal roles. Insulin promotes the storage of glucose, fatty acids, and amino acids, while glucagon stimulates mobilization of these constituents from storage into the blood. Insulin release is triggered by high blood glucose levels. It lowers blood sugar levels and inhibits the release of glucose by the liver in order to keep blood levels down. Insulin excess can cause hypoglycemia leading to convulsions or coma, and insufficient levels of insulin can cause diabetes mellitus, which can be fatal if left untreated. Diabetes mellitus is the most common endocrine disorder.
Glucagon secretion is stimulated by decreased blood glucose levels, infection, cortisol, exercise, and large protein meals. Among other activities, it facilitates glucose release into the blood. Excess glucagon can result from tumors of the pancreatic alpha cells, and a mild diabetes seems to result. Some cases of uncontrolled diabetes
The female reproductive hormones arise from the hypothalamus, the anterior pituitary, and the ovaries. Although detectable amounts of the steroid hormone estrogen are present during fetal development, at puberty estrogen levels rise to initiate secondary sexual characteristics. Gonadotropin releasing hormone (GRH) is released by the hypothalamus to stimulate pituitary release of LH and FSH, which propagate egg development in the ovaries. Eggs (ova) exist at various stages of development, with the maturation of one ovum taking about 28 days. The ova are contained within follicles that are support organs for ova maturation. About 450 of a female's 150,000 germ cells mature to leave the ovary. The hormones secreted by the ovary include estrogen, progesterone, and small amounts of testosterone.
As an ovum matures, rising estrogen levels stimulate additional LH and FSH release from the pituitary. Prior to ovulation, estrogen levels drop, and LH and FSH surge to cause the ovum to be released into the fallopian tube. The cells of the burst follicle begin to secrete progesterone and some estrogen. These hormones trigger thickening of the uterine lining, the endometrium, to prepare it for implantation should fertilization occur. The high progesterone and estrogen levels prevent LH and FSH from further secretion—thus hindering another ovum from developing. If fertilization does not occur, eight days after ovulation the endometrium deteriorates, resulting in menstruation. The falling estrogen and progesterone levels that follow trigger LH and FSH, starting the cycle all over again.
In addition to its major roles in the menstrual cycle, estrogen has a protective effect on bone loss, which can lead to osteoporosis.
Hormones related to pregnancy include human chorionic gonadotrophin (HCG), estrogen, human chorionic somatomammotrophin (HCS), and relaxin. HCG is released by the early embryo to signal implantation. Estrogen and HCS are secreted by the placenta. As birth nears, relaxin is secreted by the ovaries to relax the pelvic area in preparation for labor.
Male reproductive hormones come from the hypothalamus, the anterior pituitary, and the testes. As in females, GRH is released from the hypothalamus, which stimulates LH and FSH release from the pituitary. Testosterone levels are quite low until puberty. At puberty, rising levels of testosterone stimulate male reproductive development including secondary characteristics. LH stimulates testosterone release from the testes. FSH promotes early spermatogenesis. The male also secretes prostaglandins. These substances promote uterine contractions which help propel sperm towards an egg during sexual intercourse. Prostaglandins are produced in the seminal vesicles, and are not classified as hormones by all authorities.
Little, M. The Endocrine System. New York: Chelsea House Publishers, 1990.
Parker, M., ed. Steroid Hormone Action. New York: IRL Press, 1993.
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Author Info: , Thomson Gale, Detroit, Gale Encyclopedia of Childhood and Adolescence, 1998 |