Chapter Seventeen - The Endocrine System
I. An Overview of the Endocrine System (p. 600; Figs. 17.1, 17.2; Transp. 330; Tables 17.1, 17.4)
A. A hormone is a chemical messenger secreted by one endocrine gland or cell into the bloodstream and targeted toward cells in another organ.
B. The endocrine system is a collective term for all such hormone-secreting glands as well as the hormone-secreting cells located elsewhere.
C. The nervous and endocrine systems work together to maintain homeostasis, and use some of the same chemicals to carry out their tasks. Neurotransmitters have comparatively local effects, while the same chemical released into the bloodstream as a hormone can have a more systemic effect.
II. The Hypothalamus and Pituitary Gland (p. 602)
A. Anatomy (p. 602; Figs. 17.3, 17.4; Transp. 331)
1. The hypothalamus forms the floor and walls of the third ventricle, and regulates the body's primitive functions ranging from water balance to sex drive.
2. The pituitary (hypophysis) is protected by the sella turcica, and is attached to the hypothalamus by a stalk known as the infundibulum. The pituitary is composed of two different structures that arise independently in the embryo.
a. The adenohypophysis has two parts: the anterior lobe and the pars tuberalis. In the fetus there is also a pars intermedia.
b. The neurohypophysis has three parts: the median eminence, stalk, and the posterior lobe. The neurohypophysis is in reality a mass of nervous tissue whose somas are located in the hypothalamus. The axons form the hypothalamo-hypophyseal tract in the stalk. Hormones are made in the somas, then stored in the posterior pituitary.
B. Anterior Lobe Hormones (p. 604; Fig. 17.5; Transp. 332)
1. The anterior pituitary synthesizes and secretes six hormones.
a. Follicle-stimulating hormone (FHS) stimulates follicle and egg development in the ovaries, and sperm production in the testes.
b. Luteinizing hormone (LH) stimulates female ovulation and growth of the corpus luteum. In males, LH stimulates the testes to secrete testosterone.
c. Thyroid-stimulating hormone (TSH) or thyrotropin stimulates the thyroid to produce and secrete its hormones.
d. Adrenocorticotropic hormone (ACTH) stimulates the adrenal cortex to secrete its hormones, as well as fat catabolism in adipose tissue and insulin secretion by the pancreas.
e. Prolactin (PRL) acts on the female mammary gland to promote milk synthesis. In males, it indirectly enhances the secretion of testosterone.
f. Growth hormone (GH), or somatotropin, stimulates cellular growth, mitosis, and differentiation, promoting overall tissue and organ growth.
2. FSH and LH are gonadotropins. These two, along with TSH and ACTH are considered to be tropins.
C. The Pars Intermedia (p. 605)
1. The pars intermedia was once thought to secrete melanin-stimulating hormone, but is now known to instead give rise to anterior pituitary cells that produce pro-opiomelanocortin (POMC).
D. Posterior Lobe Hormones (p. 605; Table 17.2)
1. The posterior lobe stores and secretes two hormones manufactured in the hypothalamus.
a. Antidiuretic hormone (ADH) acts on the kidneys to increase water retention and thus prevent dehydration.
b. Oxytocin (OT) stimulates uterine labor contractions and milk release by mammary glands.
E. Control of Pituitary Secretion (p. 605)
1. Hypothalamic Control of the Anterior Lobe (p. 605; Table 17.3)
a. Timing of the secretion of pituitary hormones is controlled by the hypothalamus.
b. The hypothalamus is connected to the anterior lobe by the hypothalamohypophyseal portal system.
c. The hypothalamus secretes both releasing hormones and inhibiting hormones to regulate the release of anterior pituitary hormones.
2. Hypothalamic Control of the Posterior Lobe (p. 606)
a. The posterior pituitary is controlled by neuroendocrine reflexes; its hormones are released when signaled by nervous impulse from the hypothalamus.
b. The hypothalamus is signaled by conditions in the body as the sensory portion of this reflex.
3. Influence of Higher Brain Centers (p. 607)
a. Neuroendocrine reflexes can be modified by emotional responses, stress, and other factors.
4. Feedback from Target Organs (p. 607; Fig. 17.6; Transp. 333)
a. The target organs for pituitary hormones usually influence hormone release by negative feedback inhibition.
b. Target organs can sometimes be involved in a positive feedback cycle, as is the case with oxytocin and uterine contractions.
F. Growth Hormone (p. 608)
1. Growth hormone (GH) stimulates tissue and organ growth by promoting cellular growth, mitosis, and cellular differentiation.
a. GH achieves these effects by influencing protein synthesis, lipid metabolism, carbohydrate metabolism, and electrolyte balance.
2. GH more obviously exerts an effect of cartilage, bone, and muscle growth. A decline in GH with age, and slower rate of protein synthesis, may contribute to the aging process.
G. Pituitary Disorders (p. 608; Figs. 17.7, 17.8)
1. A number of diseases result from hyper- or hyposecretion of pituitary hormones.
a. Childhood hypopituitarism causes pituitary dwarfism, due to deficient GH. Complete loss of anterior pituitary function triggers atrophy in target organs, leading to a broad range of disorders.
b. Hyperpituitarism (of GH) in childhood causes gigantism; in adulthood, acromegaly.
c. Lack of ADH from the posterior pituitary triggers diabetes insipidus, leading to excessive urine output and electrolyte imbalances.
III. Other Endocrine Glands (p. 610)
A. The Pineal Gland (p. 610)
1. The pineal gland (epiphysis cerebri) is attached to the roof of the third ventricle. Its size regresses with age.
2. The pineal gland produces serotonin during the day, and melatonin at night. There may also be a relationship between melatonin and mood, including depression and sleep disorders.
B. The Thymus (p. 610; Fig. 17.9; Transp. 334)
1. The thymus, located in the mediastinum, undergoes involution after puberty.
2. The thymus secretes thymopoietin and thymosins that regulate the development and activation of T-lymphocytes.
C. The Thyroid (p. 610; Fig. 17.10)
1. The thyroid, located below the larynx, is the largest endocrine gland, and receives the highest rate of blood flow per gram of tissue.
2. Thyroid follicular cells secrete thryoxine (T4) and triiodothyronine (T3). Target cells convert T4 to T3. The effects of T3 on target cells increase the oxygen consumption and heat production in the cell, accounting for the calorigenic effect. This effect is stimulated by cold weather and pregnancy.
3. C cells (parafollicular cells) secrete calcitonin, a hormone that lowers blood calcium levels by promoting calcium deposition in bone.
4. Thyroid Disorders (p. 611; Fig. 17.11)
a. Congential hypothyroidism (cretinism) is caused by an inadequate supply of thyroxine from the mother. This results in skeletal system stunting, thickened facial features, low body temperature, and mental retardation.
b. Adult hypothyroidism causes myxedema, a condition characterized by low metabolic rate, weight gain, elevated blood pressure, sluggishness, and other symptoms.
c. A goiter is a pathological enlargement of the thyroid gland. Endemic goiter is due to dietary iodine insufficiency. Toxic goiter (Graves disease) is an autoimmune disease, and the person has elevated heart and metabolic rates, and associated symptoms.
D. The Parathyroids (p. 612; Fig. 17.12)
1. The parathyroids (usually four) are located on the posterior of the thyroid.
2. The parathyroids secrete parathyroid hormone (PTH) in response to hypocalcemia. PTH raises blood levels of calcium by promoting its absorption through the intestines, by inhibiting urinary excretion of calcium, and by increasing osteoclast activity.
3. Hyperparathyroidism elevates plasma levels of calcium and phosphate ions, softens bones, and causes kidney stones to develop.
E. The Adrenals (p. 613; Fig. 17.13; Transp. 335)
1. The adrenal glands are located atop the kidneys, and are retroperitoneal. They are formed from the merger of two fetal glands with different origins and functions.
2. The Adrenal Medulla (p. 613)
a. The adrenal medulla is not fully formed until the age of three, and is actually a ganglion of the sympathetic nervous system made up of modified neuron somas.
b. The medulla secretes catecholamines (epinephrine and norepinephrine) in response to sympathetic stimulation. Their effects mimic those of the sympathetic nervous system but last longer because they are secreted into the bloodstream.
3. The Adrenal Cortex (p. 613)
a. The adrenal cortex consists of three layers of modified epithelial cells: the outer zona glomerulosa, a middle zona fasciculata, and an inner zona reticularis.
b. The cortex secretes more than 25 steroid hormones (corticosteroids) that fall into three categories: sex steroids (androgens, such as DHEA), mineralocorticoids (aldosterone), and glucocorticoids (cortisol).
c. Glucocorticoid secretion, as stimulated by ACTH, stimulate fat and protein catabolism, and increase energy supplies in the bloodstream. These hormones are secreted in response to stress.
4. Adrenal Disorders (p. 614; Figs. 17.14, 17.15)
a. Hypersecretion by the adrenal medulla may be caused by a tumor (pheochromocytoma). This results in hypertension, elevated metabolic rate, hyperglycemia, nervousness, sweating, and other disorders.
b. Hypersecretion by the adrenal cortex can result from a cortical tumor or excessive ACTH. This causes Cushing syndrome, which is characterized by lost muscle and bone mass, and a redistribution of body fat.
c. Adrenogenital syndrome (AGS) is caused by hypersecretion of the adrenal androgens. Newborn girls can be mistaken for boys due to the masculinization of their genitals. Adult women also experience masculinizing effects.
d. Hyposecretion of glucocorticoids and mineralocorticoids causes Addison disease. This is characterized by darkened skin, hypoglycemia, dehydration, hypotension, weakness, and loss of stress resistance.
F. The Pancreas (p. 615; Fig. 17.16; Transp. 336)
1. The pancreas is located retroperitoneally, below and behind the stomach. Its endocrine tissue is called pancreatic islets (islets of Langerhans).
2. Pancreatic Hormones (p. 615)
a. Insulin, from beta cells, is secreted in response to rising blood levels of glucose and other nutrients. Insulin promotes the synthesis of glycogen, fat, and protein, thus lowering blood glucose levels.
b. Glucagon, from alpha cells, is secreted in response to low blood levels of glucose. It stimulates fat catabolism, glycogenolysis, and gluconeogenesis.
c. Somatostatin (from delta cells) is chemically identical to GHIH, and is secreted by the pancreas as a paracrine secretion. It diffuses to alpha and beta cells and modulates their secretion of glucagon and insulin.
3. Diabetes Mellitus (p. 615)
a. Diabetes mellitus (DM) is any disease resulting from the hyposecretion or inactivation of insulin. There are two forms of the disease: Type I and Type II.
b. Classic signs of DM are polyuria, polydipsia, and polyphagia. A blood test reveals hyperglycemia; urine tests show glycosuria and ketonuria.
c. Type I, or insulin-dependent diabetes mellitus (IDDM), results from the destruction of beta cells from an autoimmune disorder. When 90% of the beta cells are destroyed, insulin secretion falls critically low. Untreated, death can result from ketoacidosis.
d. Type II, or non-insulin-dependent diabetes mellitus (NIDDM) accounts for the majority of cases. The problem in NIDDM is insulin resistance. Target cells lack insulin receptors, and thus cannot respond to the hormone. Heredity, age, and obesity play a role in the development of NIDDM.
4. Hyperinsulinism (p. 617)
a. Hyperinsulinism occurs when a diabetic injects too much insulin. This causes rapid glucose uptake, and the person becomes hypoglycemic, weak, and hungry. When this condition goes uncorrected, it can produce insulin shock. In this instance, the brain is deprived of glucose, and disorientation, convulsions, or unconsciousness can result.
G. The Gonads (p. 617; Fig. 17.17)
1. The gonads are both exocrine and endocrine.
2. Ovarian follicles produce estradiol prior to menstruation, and progesterone afterward. The follicle asp secretes inhibin to prevent further release of FSH.
3. Interstitial cells between seminiferous tubules secrete testosterone, which stimulates development of the male reproductive system and masculine physique. Sustentacular cells of the testes secrete inhibin which also slows FSH release.
H. Endocrine Cells in Other Organs (p. 617; Table 17.4)
1. The heart secretes atrial natriuretic factor (ANF) when over stretched by high blood pressure. This increases urine output to help lower blood pressure.
2. The kidneys produce calcitrol that affects the handling of calcium by the kidneys, small intestines, and bones, and erythropoietin that stimulates bone marrow to produce more red blood cells.
3. The liver secretes somatomedians, some of the body's erythropoietin, and a prohormone, angiotensinogen.
4. The stomach and small intestine produce enteric hormones that coordinate the activities of the digestive system.
5. The placenta secretes hormones during pregnancy that regulate the pregnancy and prime the mammary glands.
IV. Hormones and Their Actions (p. 620)
A. The Chemical Identity of Hormones (p. 620; Fig. 17.18; Table 17.5)
1. Hormones fall into three major chemical classes: steroids, biogenic amines, and peptide hormones.
B. Synthesis and Transport (p. 620)
1. Steroids (p. 620; Fig. 17.19; Transp. 337)
a. Steroids are derived from cholesterol and are hydrophobic. They must bind to hydrophilic transport proteins (albumins and globulins) to be taken up by target cells.
2. Thyroid Hormones (p. 621; Fig. 17.20; Transp. 338)
a. Thyroid hormones are biogenic amines. The colloid consists of a protein called thyroglobulin to which residues of iodine can be added. Monoiodotyrosine (MIT) is formed first, then diiodotyrosine (DIT). The union of MIT and DIT forms T3; two DITs form T4.
b. Upon receipt of TSH, T4 and T3 are released into the blood. These hormones are hydrophobic and are transported by carrier proteins, one of which is thyroxine-binding globulin (TBG). Over 99% of the thyroxine is bound to carriers; only unbound T3 and T4 can enter cells. The bound form serves as a blood reservoir for the hormone.
3. Peptides (p. 623; Fig. 17.21)
a. Prohormones (inactive polypeptides) come from large precursors called preprohormones. Prohormones are cut and spliced to make active peptide hormones. Insulin is produced in this manner.
b. Most peptides are transported in the plasma as free hormones but some, such as GH, are bound to transport proteins.
C. Hormone Receptors (p. 624; Fig. 17.22; Transp. 339)
1. Hormones stimulate only those cells that have specific receptors for them. The receptors are protein or glycoprotein molecules, and the hormones are their ligands.
2. Receptor-hormone interactions are similar to enzyme-substrate interactions except the hormone is not altered chemically.
3. Receptor-hormone combinations act like switches to turn on or off certain metabolic pathways. Receptors are located either in the plasma membrane or in the nucleus, depending on whether the hormone can pass through the plasma membrane.
D. Modes of Action (p. 624)
1. The Action of Thyroid Hormones (p. 624; Fig. 17.23; Transp. 340)
a. Thyroid hormones act by directly activating genetic transmission and synthesis of new enzymes that affect cell physiology.
b. Target cells for thyroid hormones absorb free T3 and T4 and convert most of the T4 into T3 in the cytoplasm. T3 then binds to receptors in the nucleus that activate the transcription of DNA. Changes generally lead to increased metabolic rate and greater heat production. The anterior pituitary responds to T3 by producing more GH.
2. The Action of Steroids (p. 625)
a. Steroids also act by directly activating genetic transmission and synthesis of new enzymes that affect cell physiology.
b. Steroid hormones dissociate from their carriers, diffuse through membrane phospholipids, and combines with a receptor in the nucleus. The receptor has a region that binds the hormone, another to bind a chromatin acceptor site, and a third to activate DNA transcription at that site.
c. Transcription leads to the synthesis of new proteins and enzymes that alter the metabolism of the target cell.
3. The Action of Peptides and Biogenic Amines (p. 625; Figs. 17.24, 17.25; Transps. 341, 342)
a. Peptides and biogenic amines can activate or deactivate enzymes that are already present, or they can alter plasma membrane permeability and membrane potential.
b. Peptides and biogenic amines do not enter the target cell but bind to receptors on the cell surface. Their effects are exerted through second messengers, like cyclic adenosine monophosphate (cAMP).
c. Some hormones employ different second-messenger systems in different target cells.
E. Enzyme Amplification (p. 627; Fig. 17.26; Transp. 343)
1. One hormone activates thousands of enzyme molecules through enzyme amplification. This happens in the cAMP system.
2. In the cAMP system, one hormone molecule binds to a receptor, which activates many molecules of adenylate cyclase through the action of G proteins. Each adenylate cyclase makes many cAMP molecules, each of which, in turn, activates numerous molecules of protein kinase. Each protein kinase phosphorylates many enzyme molecules that each act on many molecules of substrate.
F. Effects of Hormone Concentration (p. 627; Fig. 17.27; Transp. 344)
1. Hormones influence the number of receptors in their target cells by up-regulation (increasing the number of receptors and thus, sensitivity to the hormone), or by down-regulation, caused by long-term exposure to high levels of the hormone.
G. Hormone Deactivation (p. 628)
1. Hormones must be deactivated after carrying out their tasks. The liver performs this function in less than two minutes after they have gone into circulation in the bloodstream.
H. Hormone Interactions (p. 628)
1. Hormones in circulation may have interactive effects in their target cells.
2. These effects may be synergistic, permissive (one hormone enhances the target organ's response to a second, later hormone), or antagonistic.
V. Eicosanoids and Other Chemical Messengers (p. 629; Fig. 17.28; Transp. 345)
A. Other chemical messengers exist in the body, sometimes referred to as local hormones (paracrine secretions) because they diffuse short distances and stimulate nearby cells.
B. Eicosanoids fit this description, and there are several kinds.
a. Leukotrines mediate allergic and inflammatory reactions.
b. Prostacyclin inhibits blood clotting and vasoconstriction in the blood vessels producing it.
c. Thromboxanes are made by platelets and can override the effects of prostacyclin when needed after injury.
d. Prostaglandins are produced in most or all organs of the body. The varied roles of prostaglandins are summarized in Table 17.6, p. 631.
VI. Stress and Adaptation (p. 631)
A. Hans Selye studied stress in the 1930's by injecting extracts of cattle ovary into laboratory rats. He observed what he called the general adaptation syndrome (GAS), which is broken down into three stages.
1. Stage 1 is the alarm reaction, in which CRH triggers ACTH which triggers secretion of glucocorticoids to mobilize energy sources. The alarm reaction also involves the sympathoadrenal system and fight-or-flight state.
2. Stage 2 is the state of resistance. Accelerated heartbeat, as well as elevated blood levels of glucose, glycerol, amino acids, and epinephrine are seen here. ADH levels rise, promoting sodium and water retention.
3. Stage 3 is the stage of exhaustion which occurs if stage 2 has failed to restore homeostasis. Cortisol levels are harmful over the long term, and can cause headaches, ulcers, irregular heartbeat, inhibit the immune system, and potentially lead to death.
CHAPTER ESSAY: Hormones and Circadian Rhythms (p. 632; Fig. E.1)
i. The body has its own biological clock that regulates its circadian rhythms.
ii. The biological clock consists of a pair of suprachiasmatic nuclei in the hypothalamus. Impulses end up in the pineal gland which synthesizes serotonin during daylight and melatonin at night.
iii. Night shift workers run into problems when they try to fight against their biological clock.
iv. Seasonal affective disorder (SAD) is due to lack of sunlight during winter months.
VII. Connective Issues (p. 635)
A. Interactions between the endocrine system and other organ systems are listed on p. 635.
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