GROWTH HORMONE (GH, somatotropin):
ORIGIN: Anterior pituitary gland (acidophil cells)
REGULATED BY: GH-releasing hormone (GHRH) and inhibiting hormone (somatostatin) from the hypothalamus.
FUNCTION: Promotes growth of bone and cartilage; increases protein synthesis throughout the body; promotes lipid breakdown to fatty acids, which can be use for energy; decreases the use of glucose as an energy
source, which raises blood glucose concentration and results in increased glycogen storage. GH appears to act indirectly by first inducing the liver to produce somatomedins, protein growth factors. Decreased blood levels of glucose or amino acids, as might occur in malnutrition, stimulate the pituitary to secrete GH, thereby restoring lost tissue proteins.
Another hormone, somatomammotropin, is produced by the placenta and resembles somatotropin in structure and function. By increasing maternal blood levels of glucose and fatty acids, somatomammotropin increases the availability of nutrients for the fetus.
EXCESS: Causes gigantism (symmetric) in children, and acromegaly (asymmetric growth and marked enlargement of hands, feet, forehead, jaw and other tissues) in adults.
DEFICIENCY: In children, causes symmetrical dwarfism with normal intelligence.
Fig. 11-3. Feedback loops of the pituitary gland.
PROLACTIN: ORIGIN: Anterior pituitary gland (acidophil cells) STRUCTURE: Protein
REGULATED BY: Prolactin-releasing and, especially, inhibiting hormone (PIF, prolactin inhibitory factor) from hypothalamus, which in turn are regulated by neural feedback to the hypothalamus during nursing.
FUNCTION: Stimulates milk secretion in pregnancy. NOTE: Estrogen stimulates development of the breast duct system, breast fat deposition, and breast stroma; progesterone stimulates the development of breast glandular tissue and alveoli, the secretory structures of the breast; prolactin stimulates milk secretion into the alveoli during pregnancy and nursing, whereas oxytocin stimulates breast myoepithelial cells to contract, thereby externally ejecting the milk that has been stored in the breast alveoli.
EXCESS: May occur in prolactin-producing tumors, or with excess thyroid releasing hormone (TRI1) production, which stimulates prolactin secretion in addition to TSH secretion. Galactorrhea (excess milk secretion) results, as well as amenorrhea and anovulation secondary to disturbances of the menstrual cycle. Nursing also stimulates prolactin production and hence is associated with decreased fertility during the phase of nursing. Excess prolactin in males results in testosterone deficiency and impotence.
ADRENOCORTICOTROPIC HORMONE (ACTH, corticotropin)
ORIGIN: Anterior pituitary gland (basophil cells)
REGULATED BY: Corticotropin releasing hormone (CRH) from hypothalamus, which in turn is regulated by negative feedback from blood levels of Cortisol to both the hypothalamus (decreasing CRH secretion) and anterior pituitary gland (decreasing ACTH secretion). In addition, stress itself, whether physical or mental, can trigger CRH release through neural communication to the hypothalamus.
FUNCTION: Stimulates secretion of Cortisol (a glucocorticoid) and also, to some degree, aldosterone (a mineralocorticoid) and androgenic steroids in the adrenal cortex.
EXCESS: Cushing's disease specifically refers to the clinical effects of increased ACTH secretion (and hence secondarily increased adrenal corticosteroid production) from a pituitary tumor. Cushing's syndrome is a broader term, referring to the results of excess corticosteroids, whether it be due to a primary oversecre-tion by the pituitary or adrenal, or chronic administration of corticosteroids (the most common cause). As a result of the increased output of glucocorticoids, there are obesity, buffalo hump deformity, moon-face, stria, osteoporosis, myopathy, psychosis, and diabetes from abnormalities in the metabolism and distribution of carbohydrates, proteins, and fats. The antiinflammatory effect of the glucocorticoids adds the symptoms of decreased inflammatory response. The ex-
BREAST (M I UK REUMASB
cess production of mineralocorticoids adds the symptoms of hypertension and hypokalemic alkalosis. The coinciding effects of increased androgen production include amenorrhea, hirsuitism, and acne. No wonder the patient has, on top of all this, stress ulcers—and polycythemia (excess red cell concentration), too.
DEFICIENCY: Although pituitary disease may be a cause of adrenal cortical deficiency (Addison's disease), most cases result from destruction of the adrenal cortex. Lack of aldosterone results in fluid loss that may cause hypotension, even shock and death, hyponatremia (decreased plasma sodium), hyperkalemia (high plasma potassium), and acidosis from inability of sodium to be reabsorbed in the kidney in exchange for H + . Loss of Cortisol results in muscle weakness and poor tolerance to stress, from general inability to promote gluconeogenesis and protein and fat breakdown. Increased skin pigmentation occurs in Addison's disease of adrenal destruction, possibly due to the feedback increase in ACTH, which resembles melanocyte stimulating hormone in structure and has some effect in increasing skin pigmentation. The pigmentary effect is absent in Addison's disease of pituitary origin.
LUTEINIZING HORMONE (LH) AND FOLLICLE STIMULATING HORMONE (FSH)
ORIGIN: Anterior pituitary gland (basophil cells)
REGULATED BY: Hypothalamic gonadotrophic releasing hormone (GnRH), a releasing hormone for both LH and FSH. In males, GnRH is regulated by negative feedback from blood levels of testosterone. Also, spermatogenesis is believed to decrease FSH secretion in the pituitary through inhibin, a protein hormone produced by the Sertoli cells of the testes. In females, inhibin is produced by the corpus luteum and, together with estrogen and progesterone inhibit the production of LH and FSH through interactions with the pituitary gland and hypothalamus.
FUNCTION: In males, LH stimulates testosterone synthesis in the testes Leydig cells, whereas FSH stimulates Spermatogenesis, facilitated by testes Sertoli cells. Mnemonic: FSH (fish) stimulates production of sperm (which swim like fish). (The Sertoli cells do not acutally produce sperm but facilitate the transformation of spermatids to spermatozoa. Futher maturation and motility of the spermatozoa occur on contact with the fluids of the epididymis, vas deferens, seminal vesicles, prostate gland, and bulbourethral glands. The alkalinity of the prostatic secretions, especially, contribute to activating sperm motility.)
In females, FSH, as the name implies, stimulates ovarian follicles to grow and produce estradiol. LII, as the name implies, stimulates the follicle to ovulate and mature into a corpus luteum, which secretes both estrogen and progesterone (Fig. 11-8).
THYROID STIMULATING HORMONE (TSH) (Fig. 11-3,11-4)
ORIGIN: Anterior pituitary (basophil cells) STRUCTURE: Glycoprotein REGULATION: Secretion is stimulated by hypothalamic TRH (thyrotropin-releasing hormone). In addition, thyroid hormone appears to act directly on the anterior pituitary TSH-secreting cells (and perhaps to some degree indirectly on hypothalamic TSH secretion) to suppress secretion.
FUNCTION: Controls production of thyroid hormone. Thyroid hormone is stored in the form of thy-roglobulin, a glycoprotein, in the colloid of thyroid follicles (Fig. 11-4). TSH stimulates all aspects of thyroid hormone synthesis, including the uptake of iodide, its incorporation into thyroglobulin, and the breakdown of thyroglobulin to release thyroxine (T4) and triiodothyronine (T3), the active forms of thyroid hormone, which enter the blood stream. TSH also stimulates the proliferation of the thyroglobulin-synthesizing cuboidal cells of the thyroid follicles, thereby contributing to goiter (enlarged thyroid) in cases of excess TSH production. Once in the blood stream, T3 and T4 combine with, and are transported by a glycoprotein, thyroxine-binding globulin (TBG). It is only the free-circulating hormone, as opposed to the TBG-bound portion that is metabolically active and directly enters cells. Thus, measurement of free T4 is a more reliable index of thyroid hormone function than measurement of total serum T4, which includes the TBG fraction.
Fig. 11-4. Synthesis of thyroid hormone.
MELANOCYTE STIMULATING HORMONE ORIGIN: Anterior lobe of pituitary STRUCTURE: Peptide
FUNCTION: Promotes melanin pigmentation of the skin
HYPOTHALAMIC RELEASING HORMONES: ORIGIN: Hypothalamus STRUCTURE: Peptides
FUNCTION: Stimulate release of hormones by the anterior pituitary.
ANTIDIURETIC HORMONE (ADH; vasopressin)
ORIGIN: Hypothalamus (stored in axon endings in posterior pituitary) STRUCTURE: Polypeptide
REGULATED BY: Osmotic changes in blood (Na+); neural input to hypothalamus.
FUNCTION: Acts on the kidney to promote reab-sorption of water into the blood circulation; a potent vasoconstrictor.
EXCESS: Fluid retention; hyponatremia.
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