BIO 3520 Notes, 4/24/09
ENDOCRINE SYSTEM
I. Introduction. [Widmaier, pp. 316-137]
A. The endocrine system is the second major communication system in the
body.
B. Involved in the regulation of:
1. Cardiovascular system.
2. Water and electrolyte balance.
3. Digestion and absorption of food.
4. Growth and metabolism.
5. Reproduction.
C. Gland = Group of epithelial cells specialized for secretion.
1. Derived from epithelial tissue.
2. Exocrine gland -- Secretes chemical substances into a duct
(fig. 11-1).
a. Example:
3. Endocrine gland -- Secretes chemical messengers (hormones) into
the blood.
a. Example:
D. Hormone = Chemical messenger that is secreted into the blood by
specialized cells and alters the activity of other cells in the body.
E. Some glands are both exocrine and endocrine (ex. pancreas).
F. Target cell = Cell on which a hormone exerts its effect.
1. Hormone binds to receptors in or on the target cell.
2. Receptor = Component of a cell with which a chemical messenger
(such as a hormone) combines to exert its effect.
a. Receptors are specific (fig. 5-2).
1. Not all cells contain receptors for a particular hormone.
b. Receptor activation causes changes in the activity of the target cell.
1. Example: Oxytocin stimulates contraction of smooth muscle cells
in uterus.
II. Survey of Endocrine Glands (figure, table 11-1a, 11-1b).
III. Pituitary Gland. [pp. 330-332]
A. Lies at the base of the brain, just below the hypothalamus
1. Connected by a stalk containing nerve fibers and small blood vessels.
B. Controls the activity of several other glands and organs.
C. Posterior pituitary .
1. Derived from neural tissue.
2. Secretes two hormones.
a. Antidiuretic hormone (vasopressin, ADH).
1. Permits reabsorption of water by collecting ducts.
2. Concentrates the urine.
b. Oxytocin.
1. Stimulates contraction of uterus.
2. Stimulates milk secretion.
D. Anterior pituitary.
1. Derived from epithelial tissue.
2. Produces at least six hormones (fig. 11-15, figure).
a. Stimulate other endocrine glands.
1. Thyroid-stimulating hormone (TSH) stimulates the thyroid
gland.
2. Adrenocorticotropic hormone (ACTH) stimulates the
adrenal cortex.
b. Stimulate the gonads (gonadotropins).
1. Follicle-stimulating hormone (FSH) stimulates development
of gametes.
2. Luteinizing hormone (LH) stimulates production of
sex hormones.
c. Stimulate nonendocrine tissues.
1. Growth hormone stimulates growth and affects metabolism.
2. Prolactin stimulates milk production.
3. Secretion of anterior pituitary is subject to control by hypothalamus.
IV. Hypothalamic Control of the Pituitary. [pp. 330-336]
A. Pituitary attaches to hypothalamus by a tiny stalk (figure).
B. Secretion of posterior pituitary hormones is controlled by neural
connections from hypothalamus (fig. 11-13, figure).
C. Secretion of anterior pituitary hormones is controlled by specific
releasing hormones produced by neurons in the hypothalamus
1. Produced by neurons in hypothalamus.
2. Secreted into blood, which flows directly to anterior pituitary.
3. Hormones bind to receptors on target cells in anterior pituitary.
4. Stimulate release of a specific anterior pituitary hormone.
5. Example: Gonadotropin-releasing hormone (GnRH) stimulates
secretion of both FSH and LH.
D. Hypothalamus also produces a few release-inhibiting hormones
(fig. 11-17).
V. Growth Hormone. [pp. 347-351]
A. Secreted by anterior pituitary.
B. Target organs include bone, cartilage, muscle, liver.
1. Stimulates growth of bone and cartilage.
a. GH deficiency in childhood
> dwarfism.
b. GH oversecretion in childhood
> gigantism (fig. 11-29).
c. GH oversecretion in adulthood
> acromegaly (figure).
2. Stimulates protein synthesis.
a. GH deficiency in elderly may contribute to age-related breakdown
of body structure.
3. Increases blood glucose.
C. Treatment of growth hormone abnormalities.
1. Treatment of dwarfism -- replacement therapy with human growth
hormone (hGH).
a. Hormone replacement therapy = Administration of a hormone
to a person whose natural production of that hormone is deficient.
b. Manufactured by recombinant DNA technology.
c. hGH must be injected several times per week.
2. Treatment of growth hormone oversecretion -- surgical removal of
pituitary.
VI. Thyroid Gland. [pp. 337-341, 583-585]
A. Located in throat, just below larynx (fig. 11-21a).
B. Secretes thyroxine.
1. Required for growth and development.
a. Skeleton.
b. Brain -- prenatal to 2 years old.
c. Deficiency in childhood -- cretinism.
2. Stimulates cell metabolism.
a. Increases basal metabolic rate (BMR).
C. Control of thyroxine secretion (figure).
1. Negative feedback loop involving the hypothalamus and anterior
pituitary.
2. Controlled variable is thyroxine concentration in blood.
3. Iodine is required for synthesis of thyroid hormones (fig. 11-2).
D. Diseases of the thyroid gland.
1. Goiter (fig. 11-24).
a. Enlarged thyroid gland.
b. Results from iodine deficiency.
c. Prevention --
2. Hypothyroidism.
a. Thyroxine deficiency.
b. Slowed physiologic function.
1. Fatigue.
2. Slowed speech and mental function.
3. Inability to tolerate cold.
c. Treatment -- thyroxine replacement therapy.
3. Hyperthyroidism.
a. Thyroxine oversecretion.
b. Increased rate of physiological function.
1. Insomnia, anxiety.
2. Weight loss.
3. Rapid heart rate.
4. Excess heat production, skin is flushed.
c. Exophthalmos -- protrusion of eyeballs (figure).
d. Treatment.
1. Antithyroid drugs.
2. Surgical removal of thyroid.
3. Radioactive iodine (figure).
VII. Parathyroid Glands. [pp. 353-354]
A. Four tiny glands lying behind thyroid (fig. 11-31).
B. Secrete parathyroid hormone (PTH).
1. Important for regulation of blood calcium.
2. Effects.
a. Promotes resorption of Ca++ from bone.
b. Promotes renal tubular reabsorption of Ca++.
c. Increases blood Ca++ levels
C. Feedback control of blood Ca++.
1. When blood Ca++ levels are low, secretion of PTH is stimulated.
(fig. 11-32).
VIII. Adrenal Glands. [pp. 321-322, 342-344]
A. Anatomy.
1. Cap above each kidney.
2. Composed of cortex and medulla (fig. 11-6, figure).
a. Adrenal cortex secretes steroid hormones.
b. Adrenal medulla secretes epinephrine.
B. Steroid hormones of the adrenal cortex.
1. All are derived from cholesterol.
2. Lipid-soluble -- penetrate membranes easily.
a. Bind to intracellular receptors.
3. Types (fig. 11-4).
a. Mineralocorticoids (ex. aldosterone).
1. Regulate Na+ and K+ balance.
2. Promote reabsorption of Na+ from distal tubule.
b. Glucocorticoids (ex. cortisol).
1. Increase blood glucose.
2. Essential for adaptation to stress.
c. Adrenal androgens.
a. Male sex hormones.
b. Secreted in small amounts in both males and females.
C. Epinephrine (adrenalin).
1. Secreted by adrenal medulla.
2. Primary stimulus to epinephrine secretion is activation of sympathetic n.s.
3. Effects.
a. Cardiovascular
1. Increases heart rate, stroke volume, and blood pressure.
b. Respiratory.
1. Stimulates respiratory center.
2. Relaxation of airway smooth muscle
> bronchodilation.
c. Metabolic.
1. Mobilizes energy stores for utilization.
2. Increases blood glucose.
A. Located behind stomach (fig. 15-25).
B. Both exocrine and endocrine gland.
1. Exocrine portion:
2. Endocrine portion -- clumps of cells called islets of Langerhans
(figure).
a. Secrete their products (hormones) into the blood.
b. Alpha cells secrete glucagon.
c. Beta cells secrete insulin.
d. Insulin and glucagon are peptide hormones.
C. Insulin.
1. Effects.
a. Major target organs -- liver, skeletal muscle, and adipose tissue.
b. Promotes uptake of glucose into cells of most tissues.
1. Glucose enters cells by insulin-dependent facilitated diffusion.
2. Insulin inserts GLUT-4 glucose transporters into cell
membrane (fig. 16-5).
a. In the absence of insulin, 90% of GLUT-4 transporters are
internalized into cytoplasmic vesicles.
b. Exercise also stimulates insertion of GLUT-4 into muscle
cell membranes.
3. Exception -- glucose transporters in brain function independently
of insulin.
c. Stimulates metabolic pathways which favor storage of nutrients
(fig. 16-6).
1. Formation and storage of glycogen in liver and muscle.
2. Formation and storage of fat in adipose tissue.
3. Protein synthesis.
d. Lowers blood glucose levels.
2. Feedback control of blood glucose (fig. 16-7).
a. Beta cells act as sensor and control center.
b. Primary stimulus to insulin secretion
> increased blood glucose.
c. When is insulin secretion highest?
D. Glucagon.
1. Secreted is highest between meals when blood glucose is low
(fasting state) (fig. 16-9).
2. Effects are mostly opposite to those of insulin.
a. Causes breakdown and release of stored nutrients.
b. Increases blood glucose.
c. Mobilizes energy stores for use during fasting.
1. Hyperglycemia = Abnormally high blood glucose concentration.
2. Affects 15 million Americans.
3. Type 1 (insulin-dependent).
a. Beta cells are destroyed.
b. Low levels of insulin in blood.
c. High blood glucose.
d. Juvenile onset.
4. Type 2 (noninsulin-dependent).
a. Normal or elevated levels of insulin.
b. High blood glucose.
c. Target cells are resistant to insulin.
d. Adult onset.
e. 90% of diabetics in U.S.
f. Most are overweight and lack exercise.
g. Strong genetic component.
5. Diagnosis.
a. Warning signs: Excessive urination, thirst, unexplained weight loss.
b. Fasting blood glucose > 126 mg/dl (normal = 90 - 100 mg/dl).
c. Quick screen -- urine glucose test.
E. Effects of severe, uncontrolled diabetes.
1. Decreased uptake of glucose into cells
> weight loss, resemblingstarvation.
2. Hyperglycemia.
3. Accelerated oxidation of fatty acids.
a. Accumulation of ketone bodies in blood.
b. Acetone breath.
c. Ketone bodies release H+
> metabolic acidosis.
4. Glucosuria (glucose in urine).
a. Kidneys normally conserve all glucose in body.
b. When blood glucose levels are too high, some spills over into urine.
5. Excessive urination
> related to glucose in urine.a. Leads to dehydration, thirst.
6. Hypotension, due to fluid loss.
7. Diabetic coma
> effect of hypotension, dehydration, and acidosison brain.
8. Death.
1. Remove pancreas from animal
> produces diabetes.
2. 1921 -- Frederick Banting and Charles Best extracted a hormone from
the pancreas.
3. Injected it into diabetic dogs
> lowered blood glucose (figure).
4. Named it insulin (insula = island).
5. 1922 -- Injected insulin into a severely diabetic boy.
6. 1923 Nobel prize for Banting.
G. Treatment.
1. Controlled diet.
2. Exercise -- increases sensitivity of target cells to insulin.
3. Insulin -- type 1.
a. Source -- recombinant DNA.
b. Must be injected several times a day.
4. Oral hypoglycemic drugs -- type 2.
a. Stimulate insulin secretion.
b. Increase sensitivity of target cells to insulin.
H. Consequences of insulin overdose.
1. Hypoglycemia (low blood glucose).
2. Stimulates sympathetic nervous system first.
3. Loss of consciousness -- insulin shock
> death.4. Treatment -- sugar.
I. Long-term complications of diabetes.
1. Heart disease.
2. Poor circulation.
3. Nerve damage.
4. Increased susceptibility to infections.
a. Combined with poor circulation may lead to amputations (figure).
b. Leading cause of amputations in U.S.
5. Blindness (2nd leading cause of blindness in U.S.).
6. Kidney failure.
A. Pattern of testosterone secretion (figure).
1. Secreted during the prenatal period.
2. Very little produced during childhood.
3. Large increase at onset of puberty.
4. Secretion declines late in life.
B. Effects of testosterone (table 17-3).
1. Required for reproductive function.
a. Differentiation of male reproductive tract and genitalia.
b. Growth of prostate gland and seminal vesicles.
c. Spermatogenesis.
2. Stimulation of male secondary sex characteristics.
a. Rooster's comb, deer's antlers, lion's mane.
b. Distribution of facial and body hair.
c. Balding.
d. Deepening of voice.
3. Anabolic actions.
a. Bone growth, followed by closure of growth plates.
b. Muscular development.
4. Brain and behavior.
a. Libido.
b. Aggressive behavior.
C. Control of testosterone secretion (fig. 17-11).
1. Testosterone secretion is controlled by a negative feedback loop
involving the hypothalamus and pituitary.
2. Controlled variable is the testosterone concentration in blood.
3. Cells of the testes.
a. Leydig cells secrete testosterone.
b. Sertoli cells support sperm production.
4. Pituitary hormones.
a. Luteinizing hormone (LH) stimulates testosterone secretion.
b. Follicle-stimulating hormone (FSH) and testosterone
required for spermatogenesis.
c. FSH and LH secretion are stimulated by gonadotropin-releasing
hormone (GnRH) secreted by hypothalamus.
5. What is the effect of castration on FSH levels?
D. Abuse of anabolic steroids.
1. Benefits.
a. Increase muscle mass.
b. Probably improve performance.
2. Side effects.
a. Temporary sterility (explain).
b. Liver damage (hepatitis, liver cancer).
c. Heart disease.
d. Aggressive behavior.
e. Premature puberty.
f. Masculinization of women.
XI. Ovaries. [pp. 620-627, 638-640]
A. Produce female sex hormones -- estrogen and progesterone.
B. Pattern of estrogen and progesterone secretion.
1. Secretion begins at puberty.
2. Secreted in a cyclic manner until menopause (late 40's to early 50's)
(fig. 17-18).
3. Elevated during pregnancy (fig. 17-29).
4. Very low levels after menopause.
C. Effects of estrogen (table 17-8).
1. Required for reproductive function.
a. Maturation of female reproductive tract (at puberty).
b. Cyclic changes in uterus (along with progesterone).
c. Maturation of ovarian follicles.
2. Stimulation of female secondary sex characteristics.
a. Distribution of fat.
b. Development of mammary glands.
3. Anabolic actions.
a. Bone growth, followed by closure of growth plates.
b. Loss of bone mass after menopause -- osteoporosis (figure).
4. Brain and behavior.
a. Sexually receptive behavior in some species.
D. Control of estrogen secretion (fig. 17-20).
1. Estrogen secretion is under negative feedback control early in the
menstrual cycle.
2. Switches to a positive feedback loop in mid-cycle, triggering the
LH surge.
1. Follicle-stimulating hormone (FSH) and luteinizing hormone
(LH) stimulate estrogen secretion and growth of ovarian follicles.
a. Estrogen is also required for follicle growth.
2. FSH and LH secretion are stimulated by gonadotropin-releasing
hormone (GnRH) secreted by hypothalamus.
E. Review of functions of the gonadotropins.
1. Males.
a. _______ is required for spermatogenesis.
b. _______ stimulates testosterone secretion.
2. Females.
a. Both ______ and ______ are required for production of estrogen.
b. _______ stimulates growth and maturation of ovarian follicles.
c. Midcycle ______ surge triggers ovulation.
1. Sources.
a. Ovary -- during last half of menstrual cycle.
b. Placenta.
2. Effects of progesterone (table 17-8).
a. Primary function -- To prepare and maintain the proper
environment for pregnancy.
b. Cyclic changes in uterine lining.
1. Uterine lining (endometrium) becomes thick, spongy, and
full of blood vessels.
2. Prepared for implantation of fertilized egg.
3. Withdrawal of progesterone late in the cycle triggers
menstruation.
c. Development of mammary glands.
d. Inhibits ovulation.
3. Progestins -- synthetic progesterone-like hormones.
a. Important component of oral contraceptives.
1. Inhibits ovulation.
2. Withdrawal triggers menstruation.
b. Progestin-only contraceptive preparations.
1. Norplant contraceptive implant.
a. Contains synthetic progestin.
b. Lasts 5 years.
c. More than 99% effective.
d. Effects are reversed upon removal.
e. Major side effect
> irregular menstrual bleeding.f. Difficulties with removal.
2. Depo-Provera.
a. Synthetic progestin injected in slow-release form.
b. Lasts 90 days.
c. Same effectiveness and side effects as Norplant.
3. Emergency contraception.
a. Plan B -- Two pills containing synthetic progestin.
b. Take within 3 days of unprotected intercourse.
c. Interferes with ovulation, fertilization, and implantation.
d. 89% effective.
4. RU-486 (mifepristone).
a. Antiprogesterone -- blocks progesterone receptors.
b. Induces menstruation, even if pregnant.
c. Emergency contraception -- prevents implantation of fertilized
ovum.
d. Use as abortion pill in combination with a prostaglandin, which
stimulates uterine contractions.
