|Index to this page|
The Anterior Lobe
|Link to graphic showing the location|
of the pituitary and other endocrine
Some people develop antibodies against their own TSH receptors. When these bind the receptors, they "fool" the cell into making more T4 causing hyperthyroidism. The condition is called thyrotoxicosis or Graves' disease.
A deficiency of TSH causes hypothyroidism: inadequate levels of T4 (and thus of T3 [Link]).
Physicians occasionally encounter patients who are homozygous for mutant TSH receptors or mutant TRH receptors. In either case, they suffer from hypothyroidism.
A deficiency of TSH, or mutant TSH receptors, have also been implicated as a cause of osteoporosis. Mice, whose TSH receptors have been knocked out, develop increased numbers of bone-reabsorbing osteoclasts.
In sexually-mature females, FSH (assisted by LH) acts on the follicle to stimulate it to release estrogens.FSH produced by recombinant DNA technology (Gonal-f®) is available to promote ovulation in women planning to undergo in vitro fertilization (IVF) and other forms of assisted reproductive technology.
LH in males is also known as interstitial cell stimulating hormone (ICSH).
|Discussion of the negative-feedback loops that control the levels of estrogen, progesterone, and testosterone.|
After birth, prolactin promotes the synthesis of milk.Prolactin secretion is
In pregnant mice, prolactin stimulates the growth of new neurons in the olfactory center of the brain.
Things that can go wrong.
GH from domestic mammals like cows and pigs does not work in humans. So for many years, the only source of GH for therapy was that extracted from the glands of human cadavers. But this supply was shut off when several patients died from a rare neurological disease attributed to contaminated glands [Link].Now, thanks to recombinant DNA technology, recombinant human GH (rHGH) is available. While a benefit to patients suffering from GH deficiency or the short stature associated with Turner syndrome, there has also been pressure to use it to stimulate growth in youngsters who have no deficiency but whose parents want them to grow up tall. And so, in the summer of 2003, the U.S. FDA approved the use of human growth hormone (HGH) for
ACTH is a peptide of 39 amino acids. It is cut from a larger precursor proopiomelanocortin (POMC).ACTH acts on the cells of the adrenal cortex, stimulating them to produce
Production of ACTH depends on the intermittent arrival of corticotropin-releasing hormone (CRH) from the hypothalamus.
Hypersecretion of ACTH is a frequent cause of Cushing's syndrome.
MSH is discussed in a separate page. Link to it.
Vasopressin is a peptide of 9 amino acids (Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly). It is also known as arginine vasopressin (AVP) and the antidiuretic hormone (ADH).
Vasopressin acts on the collecting ducts of the kidney to facilitate the reabsorption of water into the blood. Thus it acts to reduce the volume of urine formed (giving it its name of antidiuretic hormone).
|Link to discussion of kidney physiology.|
Another type of receptor for vasopressin (designated V1a) is found in the brain, e.g., in voles and mice (rodents) and in primates like monkeys and humans.
Meadow voles whose brains have been injected with a vector causing increased expression of the V1a receptor become more like prairie voles in their behavior. (See Lim, M. M. et al., Nature, 17 June 2004.)
The level of expression of the V1a receptor gene is controlled by a "microsatellite" region upstream (5') of the ORF. This region contains from 178 to 190 copies of a repeated tetranucleotide (e.g., CAGA). Prairie voles have more copies of the repeat than meadow voles, and they express higher levels of the receptor in the parts of the brain associated with these behaviors. A similar microsatellite region is present in the pygmy chimpanzee or bonobo (Pan paniscus) but is much shorter in the less-affectionate common chimpanzee (Pan troglodytes).
|Link to a discussion of some human diseases caused by trinucleotide repeats.|
Vasopressin and the Circadian Clock
Mice are nocturnal and become active at the start of the night. This is a circadian rhythm that persists for a time even after the lights in the lab are turned off each day 8 hours sooner (like arriving in London after a flight from Los Angeles, California). Only after 8–10 days do the mice overcome their "jet lag", adjusting to the new dark-light schedule. (It also takes us about one day to reset our circadian rhythms for each hour that our day-night schedule is shifted.)
It turns out that arginine vasopressin, acting on the suprachiasmatic nucleus (SCN), plays a role in this resistance to resetting their circadian clock. Mice with their genes for the V1a and V1b receptors knocked out adjust much more quickly (2–4 days) to the change. What evolutionary advantage this resistance to resetting the circadian clock confers is not clear, but understanding the mechanism raises the possibility of using drugs to speed getting over jet lag and also to help those whose work shifts are periodically altered. (Read about this work in Yamaguchi, Y., et al. in the 4 October 2013 issue of Science.)
Oxytocin is a peptide of 9 amino acids (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly).It acts on certain smooth muscles:
Oxytocin is often given to prospective mothers to hasten birth.In rodents, oxytocin also acts on the nucleus accumbens and amygdala in the brain where it enhances:
In mice, oxytocin acts on striated muscle stem cells to promote repair after they have been injured.
In humans, oxytocin increases the level of one's trust in other people.