Chapter 18. The endocrine system
At the end of this section you can:
- Explain how hormones regulate the excretory system
- Discuss the role of hormones in the reproductive system
- Describe how hormones regulate metabolism
- Explain the role of hormones in various diseases
Hormones have a wide spectrum of effects and modulate many different bodily processes. The main regulatory processes studied here concern the excretory system, the reproductive system, metabolism, blood calcium concentration, growth and the stress response.
Hormonal regulation of the excretory system
Maintaining adequate water balance in the body is important to avoid becoming dehydrated or overhydrated (hyponatraemia). The water concentration of the body is monitored by Osmorezeptorenin the hypothalamus, which detect the concentration of electrolytes in the extracellular fluid. Electrolyte concentration in the blood increases with water loss from excessive sweating, insufficient water intake, or low blood volume from blood loss. An increase in blood electrolyte levels results in a neuronal signal sent by the osmoreceptors in the nuclei of the hypothalamus. The pituitary gland has two components: anterior and posterior. The anterior pituitary consists of glandular cells that secrete protein hormones. The posterior pituitary is an extension of the hypothalamus. It consists largely of neurons related to the hypothalamus.
The hypothalamus produces a polypeptide hormone known as Antidiuretisches Hormon (ADH), which is transported to the posterior pituitary gland and released from there. The main effect of ADH is to regulate the amount of water excreted by the kidneys. Since ADH (also known as vasopressin) causes water to be absorbed directly from the renal tubules, salts and wastes are concentrated in what is eventually excreted as urine. The hypothalamus controls the mechanisms of ADH secretion, either by regulating blood volume or the concentration of water in the blood. Dehydration or physiological stress can cause osmolarity to rise above 300 mOsm/L, which in turn increases ADH secretion and retains water, leading to an increase in blood pressure. ADH travels through the bloodstream to the kidneys. Once in the kidneys, ADH alters the kidneys to make them more permeable to water by temporarily inserting water channels, aquaporins, into the renal tubules. Water moves from the renal tubules through the aquaporins, reducing urine volume. The water is reabsorbed into the capillaries and lowers blood osmolarity back to normal. When blood osmolarity decreases, a negative feedback mechanism reduces osmoreceptor activity in the hypothalamus and ADH secretion is reduced. ADH release can be decreased by certain substances, including alcohol, which can lead to increased urine production and dehydration.
Chronic underproduction of ADH or a mutation in the ADH receptor causes it Diabetes insipidus. When the posterior pituitary does not release enough ADH, water cannot be retained by the kidneys and is lost as urine. This leads to increased thirst, but absorbed water is lost again and must be drunk continuously. If the condition is not severe, dehydration may not occur, but severe cases can lead to electrolyte imbalances due to dehydration.
Another hormone responsible for maintaining electrolyte levels in extracellular fluids is Aldosterone, a steroid hormone produced by the adrenal cortex. Unlike ADH, which promotes reabsorption of water to maintain proper water balance, aldosterone maintains proper water balance by increasing Na+resorption and K+Secretion from extracellular fluid of cells in renal tubules. Because it is produced in the cortex of the adrenal gland and affects the concentrations of the minerals Na+and k+, aldosterone is referred to as a Mineralocorticoid, a corticosteroid that affects ion and water balance. The release of aldosterone is stimulated by a decrease in blood sodium levels, blood volume or blood pressure, or by an increase in blood potassium levels. It also prevents the loss of Na+from sweat, saliva and gastric juice. The absorption of Na+also leads to osmotic reabsorption of water, which alters blood volume and blood pressure.
Aldosterone production can be stimulated by low blood pressure, triggering a series of chemical releases as shown inFigure 18.7. When blood pressure falls, the renin-angiotensin-aldosterone system (RAAS) is activated. This is recognized and released by cells in the juxtaglomerular apparatus, which regulates the functions of the kidney's nephrons Renin. Renin, an enzyme, circulates in the blood and reacts with a plasma protein made by the liver called angiotensinogen. When angiotensinogen is cleaved by renin, angiotensin I is produced, which is then converted to angiotensin II in the lungs. Angiotensin II acts as a hormone and then causes the adrenal cortex to secrete the hormone aldosterone, causing an increase in Na+reabsorption, water retention and an increase in blood pressure. In addition to being a potent vasoconstrictor, angiotensin II causes an increase in ADH and increased thirst, both of which help increase blood pressure.
Hormonal regulation of the reproductive system
The regulation of the reproductive system is a process that requires the action of hormones from the pituitary, adrenal cortex and gonads. During puberty, in both males and females, the hypothalamus produces gonadotropin-releasing hormone (GnRH), which stimulates the production and release of gonadotropin Follicle Stimulating Hormone (FSH)and luteinizing hormone (LH) from the anterior pituitary gland. These hormones regulate the gonads (testicles in men and ovaries in women) and are therefore called Gonadotropins. In both males and females, FSH stimulates gamete production and LH stimulates the production of hormones by the gonads. An increase in gonadal hormone levels inhibits GnRH production through a negative feedback loop.
Regulation of the male reproductive system
In men, FSH stimulates sperm maturation. FSH production is inhibited by the hormone inhibin, which is secreted by the testicles. LH stimulates the production of sex hormones (Androgens)through the interstitial cells of the testicles and is therefore also called interstitial cell-stimulating hormone.
The most well-known androgen in men is testosterone. Testosterone promotes sperm production and male characteristics. The adrenal cortex also produces small amounts of testosterone precursors, although the role of this additional hormone production is not fully understood.
The dangers of synthetic hormones
Some athletes try to increase their performance by using artificial hormones that increase muscle performance. Anabolic steroids, a form of the male sex hormone testosterone, are among the best-known performance-enhancing drugs. Steroids are used to help build muscle mass. Other hormones used to increase athletic performance include erythropoietin, which triggers red blood cell production, and human growth hormone, which can help build muscle mass. Most performance-enhancing drugs are illegal for non-medical purposes. They are also banned by national and international governing bodies, including the International Olympic Committee, the U.S. Olympic Committee, the National Collegiate Athletic Association, Major League Baseball and the National Football League.
The side effects of synthetic hormones are often significant and irreversible, and in some cases fatal. Androgens lead to several complications such as liver dysfunction and liver tumors, enlargement of the prostate, difficulty urinating, premature closure of the epiphyseal cartilage, testicular atrophy, infertility and depression of the immune system. The physiological burden caused by these substances is often greater than what the body can handle, resulting in unpredictable and dangerous effects and their use has been linked to heart attacks, strokes and impaired cardiac function.
Regulation of the female reproductive system
In women, FSH stimulates the development of egg cells called ova, which develop into structures called follicles. Follicular cells produce the hormone inhibin, which inhibits FSH production. LH also plays a role in oocyte development, ovulation induction, and stimulation of estradiol and progesterone production by the ovaries, as shown in Figure 18.9. Estradiol and progesterone are steroid hormones that prepare the body for pregnancy. Estradiol creates secondary sex characteristics in women, while both estradiol and progesterone regulate the menstrual cycle.
In addition to producing FSH and LH, the front part of the pituitary gland also produces the hormone Prolactin (PRL)in females. Prolactin stimulates milk production from the mammary glands after birth. Prolactin levels are regulated by hormones in the hypothalamus Prolactin-Releasing-Hormone (PRH)and Prolactin-hemmendes hormone (PIH), which is now known as dopamine. PRH stimulates the release of prolactin and PIH inhibits it.
The posterior pituitary gland releases the hormone Oxytocin, which stimulates uterine contractions during childbirth. Uterine smooth muscle is not very sensitive to oxytocin until late in pregnancy, when the number of oxytocin receptors in the uterus peaks. The stretching of tissues in the uterus and cervix stimulates the release of oxytocin during labor. The intensity of the contractions increases as blood oxytocin levels rise via a positive feedback mechanism until labor is complete. Oxytocin also stimulates the contraction of the myoepithelial cells surrounding the milk-producing mammary glands. When these cells contract, milk is pushed out of the secretory alveoli into the milk ducts and expelled from the breasts by the milk ejection reflex ("void reflex"). The release of oxytocin is stimulated by an infant's suckling, which triggers the synthesis of oxytocin in the hypothalamus and its release into the circulation at the posterior pituitary gland.
Hormonal regulation of metabolism
Blood sugar levels fluctuate widely throughout the day as periods of eating alternate with periods of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining blood sugar homeostasis. Additional regulation is mediated by the thyroid hormones.
Regulation of blood sugar levels by insulin and glucagon
Cells in the body need nutrients to function, and these nutrients are obtained through feeding. To control nutrient absorption, store excess and use reserves when needed, the body uses hormones to moderate energy stores. Insulinis produced by the beta cells of the pancreas, which are stimulated to release insulin when blood sugar levels rise (e.g. after eating a meal). Insulin lowers blood sugar levels by increasing the rate of glucose uptake and utilization by target cells that use glucose for ATP production. It also stimulates the liver to convert glucose into glycogen, which is then stored by cells for later use. Insulin also increases the transport of glucose into certain cells, such as muscle cells and the liver. This results from an insulin-mediated increase in the number of glucose transport proteins in cell membranes, which remove glucose from the circulation by facilitated diffusion. When insulin binds to its target cell via insulin receptors and signal transduction, it causes the cell to incorporate glucose transport proteins into its membrane. This allows glucose to enter the cell where it can be used as an energy source. This doesn't happen in all cells, however: some cells, including those in the kidneys and brain, can access glucose without insulin. Insulin also stimulates the conversion of glucose into fat in adipocytes and the synthesis of proteins. These insulin-mediated effects result in a drop in blood glucose concentrations, referred to as the hypoglycemic "low sugar" effect, which inhibits further insulin release from the beta cells through a negative feedback loop.
concept in action
ThisAnimationdescribe the role of insulin and the pancreas in diabetes.
Impaired insulin function can lead to what is known as a condition Diabetes Mellitus, whose main symptoms are shown in Figure 18.10. This can be caused by low insulin production by the beta cells in the pancreas or by reduced sensitivity of the tissue cells to insulin. This prevents glucose from being absorbed by cells, leading to high blood sugar levels, or Hyperglycemia(high sugar). High blood glucose levels make it difficult for the kidneys to recover all of the glucose from nascent urine, causing glucose to be lost in the urine. High glucose levels also cause less water to be reabsorbed by the kidneys, causing large amounts of urine to be produced; this can lead to dehydration. Over time, high blood sugar levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system. Oversecretion of insulin can lead to this hypoglycemia, low blood sugar level. This leads to insufficient glucose availability to the cells, often leading to muscle weakness and sometimes leading to unconsciousness or death if left untreated.
When blood sugar levels fall below normal levels, for example between meals or when glucose is used up quickly during exercise, the hormone becomes Glucagonis released from the alpha cells of the pancreas. Glucagon increases blood sugar levels and triggers what is known as a hyperglycemic effect by stimulating the breakdown of glycogen into glucose in skeletal muscle cells and liver cells in a process called Glycogenolysis. Glucose can then be used as energy by muscle cells and released into the circulatory system by liver cells. Glucagon also stimulates the uptake of amino acids from the blood by the liver, which then converts them into glucose. This process of glucose synthesis is called Glukoneogenese. Glucagon also stimulates fat cells to release fatty acids into the blood. These glucagon-mediated effects cause blood glucose levels to rise to normal homeostatic levels. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in Figure 18.11.
Pancreatic tumors can cause excessive secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin. Which of the following statements about these two conditions is correct?
- A pancreatic tumor and type 1 diabetes have opposite effects on blood sugar levels.
- A pancreatic tumor and type 1 diabetes both cause hyperglycemia.
- A pancreatic tumor and type 1 diabetes both cause hypoglycemia.
- Both pancreatic tumors and type I diabetes result in an inability of cells to take up glucose.
Regulation of blood sugar levels by thyroid hormones
The basal metabolic rate, i.e. the amount of calories that the body needs at rest, is determined by two hormones produced by the thyroid gland: thyroxine, also known as tetraiodothyronine or T4, and Trijodthyronin, also known as T3. These hormones affect almost every cell in the body except for the adult brain, uterus, testicles, blood cells, and spleen. They are transported across the plasma membrane of target cells and bind to receptors on the mitochondria, resulting in increased ATP production. At its core, T3and t4Activate genes involved in energy production and glucose oxidation. This results in increased metabolic rate and body heat production, which is known as the hormone's caloric effect.
T3and t4Release from the thyroid is stimulated by Thyroid Stimulating Hormone (TSH), which is produced by the anterior pituitary gland. TSH binding to the thyroid follicle receptors triggers the production of T3and t4from a glycoprotein called thyroglobulin. Thyroglobulin is present in the follicles of the thyroid gland and is converted into thyroid hormones with the addition of iodine. Iodine is formed from iodide ions that are actively transported from the bloodstream to the thyroid follicle. A peroxidase enzyme then binds the iodine to the tyrosine amino acid found in thyroglobulin. T3has three bound iodine ions, while T4bound four iodine ions. T3and t4are then released into the bloodstream, where T4released in much larger quantities than T3. Als T3is more active than T4and is responsible for most of the effects of thyroid hormones, tissues of the body convert T4to T3by removing an iodine ion. Most of the published T3and t4binds to transport proteins in the bloodstream and is unable to cross the plasma membrane of cells. These protein-bound molecules are only released when blood levels of the unbound hormone begin to fall. In this way, the reserve hormone is kept in the blood for a week. Increased T3and t4-Levels in the blood inhibit the release of TSH, resulting in lower TSH3and t4Release from the thyroid.
The follicular cells of the thyroid gland need iodide (iodine anions) to produce T3and t4. Iodides obtained from food are actively transported into the follicle cells, resulting in a concentration about 30 times higher than in the blood. The typical diet in North America provides more iodine than required due to the addition of iodide to table salt. Inadequate iodine intake, which occurs in many developing countries, results in an inability to absorb T3and t4hormones. The thyroid gland enlarges in what is called a condition goiter, which is caused by an overproduction of TSH without the formation of thyroid hormones. Thyroglobulin is contained in a liquid called colloid, and TSH stimulation causes higher accumulation of colloid in the thyroid. In the absence of iodine, it is not converted into thyroid hormone, and colloid begins to build up more and more in the thyroid, resulting in goiter.
Disorders can arise from both underproduction and overproduction of thyroid hormones. hypothyroidism, an underproduction of thyroid hormones, can cause a low metabolic rate, which leads to weight gain, sensitivity to cold and reduced mental activity, among other things. In children, hypothyroidism can cause cretinism, which can lead to mental retardation and stunted growth. hyperthyroidism, the overproduction of thyroid hormones, can lead to increased metabolic rate and its effects: weight loss, excessive heat production, sweating and an increased heart rate. Graves' disease is an example of an overactive thyroid.
Hormonal control of blood calcium levels
The regulation of the calcium concentration in the blood is important for the generation of muscle contractions and nerve impulses that are electrically stimulated. When calcium levels get too high, membrane permeability to sodium decreases and membranes become less reactive. When calcium levels get too low, membrane permeability to sodium increases and cramps or muscle spasms may occur.
The level of calcium in the blood is regulated by Parathormon (PTH), which is produced by the parathyroid glands, as shown in Figure 18.12. PTH is released in response to low levels of Ca in the blood2+levels. PTH increased Approx2+levels by targeting the skeleton, kidneys, and intestines. In the skeleton, PTH stimulates osteoclasts, causing bone to be resorbed and Ca to be released2+from bone to blood. PTH also inhibits osteoblasts and reduces Ca2+deposits in the bone. In the gut, PTH increases dietary Ca2+absorption and in the kidneys, PTH stimulates reabsorption of CA2+. While PTH acts directly on the kidneys to increase Ca2+Reabsorption, its effects on the gut are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the gut to increase the absorption of dietary calcium. The release of PTH is inhibited by rising calcium levels in the blood.
Hyperparathyroidism results from an overproduction of parathyroid hormone. This causes excess calcium to be removed from the bones and introduced into the bloodstream, causing structural weakness in the bones that can lead to deformities and fractures, as well as nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, leads to extremely low levels of calcium in the blood, which leads to impaired muscle function and can lead to tetany (severe sustained muscle contraction).
The hormone Calcitonin, which is produced by the parafollicular or C-cells of the thyroid gland, has the opposite effect on blood calcium levels as PTH. Calcitonin lowers blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy, nonpregnant, nonstarved adults, the role of calcitonin is unclear.
Hormonal regulation of growth
Hormonal regulation is required for the growth and replication of most cells in the body. growth hormone (GH), which is produced by the anterior part of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bone. Growth hormone has direct and indirect mechanisms of action. The first direct effect of GH is to stimulate triglyceride breakdown (lipolysis) and release into the blood by adipocytes. This results in a switch from using glucose as an energy source to using fatty acids in most tissues. This process is called a glucose-sparing effect. In another direct mechanism, GH stimulates the breakdown of glycogen in the liver; the glycogen is then released into the blood as glucose. Blood sugar levels rise because most tissues use fatty acids instead of glucose for their energy needs. The GH-mediated rise in blood sugar levels is denoted as a diabetogenic effectbecause it is similar to the high blood sugar levels in diabetes mellitus.
The indirect mechanism of GH action is mediated by insulin-like growth factors (IGFs)or somatomedins, a family of growth-promoting proteins produced by the liver that stimulate tissue growth. IGFs stimulate the uptake of amino acids from the blood and allow the formation of new proteins, particularly in skeletal muscle cells, cartilage cells, and other target cells, as shown in Figure 18.13. This is especially important after a meal when blood glucose and amino acid levels are high. GH levels are regulated by two hormones produced by the hypothalamus. This stimulates GH release Growth Hormone-Releasing Hormone (GHRH)and is inhibited by Growth Hormone Inhibitory Hormone (GHIH), also called somatostatin.
A balanced production of growth hormone is crucial for proper development. Underproduction of GH in adults does not appear to cause abnormalities, but it can cause it in children Pituitary Dwarfismwhere growth is reduced. Pituitary dwarfism is characterized by symmetrical body formation. In some cases individuals are under 30 inches tall. Oversecretion of growth hormone can lead to this gigantismin children, leading to excessive growth. In some documented cases, individuals can reach heights of over 8 feet (2.40 m). In adults, excessive GH can cause it Acromegaly, a condition in which there is enlargement of bones in the face, hands and feet that are still capable of growing.
Hormonal regulation of stress
When a threat or danger is perceived, the body responds by releasing hormones that prepare it for the "fight-or-flight" response. The effects of this reaction are well known to anyone who has been in a stressful situation: increased heart rate, dry mouth and stand-up hair.
fight or flight response
The interactions of endocrine hormones have evolved to ensure that the body's internal environment remains stable. Stressors are stimuli that disrupt homeostasis. The sympathetic division of the vertebrate autonomic nervous system has evolved the fight-or-flight response to counteract stress-induced disturbances in homeostasis. In the initial alarm phase, the sympathetic nervous system stimulates an increase in energy levels through increased blood sugar levels. This prepares the body for physical activity, which may be required to respond to stress: either to fight for survival or to flee danger.
However, some stresses, such as illness or injury, can last for a long time. Glycogen reserves, which provide energy in the short-term response to stress, are depleted after several hours and can no longer meet long-term energy needs. If glycogen reserves were the only available source of energy, neural function could not be sustained once reserves were depleted due to the nervous system's high demand for glucose. In this situation, the body has developed a response to counteract long-term stress through the action of glucocorticoids, which ensure that long-term energy needs can be met. The glucocorticoids mobilize lipid and protein reserves, stimulate gluconeogenesis, conserve glucose for use by neural tissue, and stimulate salt and water conservation. The mechanisms for maintaining homeostasis described here are those observed in the human body. However, the fight-or-flight response exists in some form in all vertebrates.
The sympathetic nervous system regulates the stress response via the hypothalamus. Stressful stimuli cause the hypothalamus to send signals via nerve impulses to the adrenal medulla (which mediates short-term stress responses) and via hormone to the adrenal cortex, which mediates long-term stress responses Adrenocorticotropes Hormon (ACTH), which is produced by the anterior pituitary gland.
Short term stress response
In a stressful situation, the body reacts by demanding the release of hormones that provide an energy boost. The hormones Adrenalin(aka adrenaline) and Norepinephrine(also known as norepinephrine) are released by the adrenal medulla. How do these hormones provide an energy boost? Epinephrine and norepinephrine raise blood sugar levels by stimulating the liver and skeletal muscle to break down glycogen and by stimulating the release of glucose by liver cells. In addition, these hormones increase oxygen availability to cells by increasing heart rate and dilating bronchioles. The hormones also prioritize bodily function by increasing blood flow to vital organs like the heart, brain, and skeletal muscles, while restricting blood flow to organs that aren't immediately needed, like the skin, digestive system, and kidneys. Epinephrine and norepinephrine are collectively called catecholamines.
concept in action
look at that
Discovery Channel-AnimationDescription of the flight-or-flight response.
Long-term stress response
The long-term stress response differs from the short-term stress response. The body cannot long sustain the energy surges mediated by epinephrine and norepinephrine. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. ACTH stimulates the adrenal cortex to release so-called steroid hormones Corticosteroids. Corticosteroids turn on the transcription of certain genes in the nuclei of target cells. They change the enzyme concentrations in the cytoplasm and influence cell metabolism. There are two main corticosteroids: Glucocorticoids such as Cortisoland mineral corticoids such as aldosterone. These hormones target the breakdown of fat into fatty acids in adipose tissue. The fatty acids are released into the bloodstream for other tissues to use in ATP production. That Glucocorticoidmainly affect glucose metabolism by stimulating glucose synthesis. Glucocorticoids also have anti-inflammatory properties by inhibiting the immune system. For example, cortisone is used as an anti-inflammatory drug; however, it cannot be used permanently, as it increases susceptibility to disease due to its immunosuppressive effects.
Mineralocorticoids regulate the body's ion and water balance. The hormone aldosterone stimulates the reabsorption of water and sodium ions in the kidneys, leading to an increase in blood pressure and volume.
Hypersecretion of glucocorticoids can cause a condition known as Morbus Cushing, characterized by a shift in fat storage areas of the body. This can lead to accumulation of fatty tissue in the face and neck and excess glucose in the blood. Hyposecretion of the corticosteroids can lead to this Addison's disease, which can cause tanning of the skin, hypoglycemia, and low levels of electrolytes in the blood.
Water levels in the body are controlled by antidiuretic hormone (ADH), which is produced in the hypothalamus and triggers the reabsorption of water by the kidneys. Underproduction of ADH can cause diabetes insipidus. Aldosterone, a hormone produced by the adrenal cortex of the kidneys, increases Na+Reabsorption from the extracellular fluids and subsequent water reabsorption by diffusion. The renin-angiotensin-aldosterone system is one way to control aldosterone release.
The reproductive system is controlled by the gonadotropins follicle stimulating hormone (FSH) and luteinizing hormone (LH) produced by the pituitary gland. The release of gonadotropin is controlled by the hypothalamic hormone gonadotropin-releasing hormone (GnRH). FSH stimulates sperm maturation in men and is inhibited by the hormone inhibin, while LH stimulates the production of the androgen testosterone. FSH stimulates egg maturation in women, while LH stimulates the production of estrogens and progesterone. estrogensare a group of steroid hormones produced by the ovaries that trigger the development of secondary sex characteristics in women and control egg maturation. In women, the pituitary gland also produces prolactin, which stimulates milk production after childbirth, and oxytocin, which stimulates uterine contraction during labor and milk secretion during suckling.
Insulin is produced by the pancreas in response to rising blood glucose levels, allowing cells to utilize blood glucose and store excess glucose for later use. Diabetes mellitus is caused by decreased insulin activity and causes high blood sugar levels or hyperglycemia. Glucagon is released by the pancreas in response to low blood sugar and stimulates the breakdown of glycogen into glucose for use by the body. The body's basal metabolic rate is regulated by the thyroid hormone thyroxine (T4) und Trijodthyronin (T3). The anterior pituitary produces thyroid-stimulating hormone (TSH), which stimulates the release of T3and t4from the thyroid. Iodine is necessary for the production of thyroid hormones, and lack of iodine can lead to a condition called goiter.
Parathyroid hormone (PTH) is produced by the parathyroid glands in response to low levels of Ca in the blood2+levels. The parafollicular cells of the thyroid produce calcitonin, which reduces Ca in the blood2+levels. Growth hormone (GH) is produced by the anterior pituitary gland and controls the growth rate of muscles and bones. GH action is indirectly mediated by insulin-like growth factors (IGFs). Short-term stress causes the hypothalamus to trigger the adrenal medulla to release epinephrine and norepinephrine, which trigger the fight or flight response. Long-term stress causes the hypothalamus to trigger the anterior pituitary gland to release adrenocorticotropic hormone (ACTH), which causes the release of corticosteroids, glucocorticoids, and mineralocorticoids from the adrenal cortex.
- Pancreatic tumors can cause excessive secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin. Which of the following statements about these two conditions is correct?
- A pancreatic tumor and type 1 diabetes have opposite effects on blood sugar levels.
- A pancreatic tumor and type 1 diabetes both cause hyperglycemia.
- A pancreatic tumor and type 1 diabetes both cause hypoglycemia.
- Both pancreatic tumors and type I diabetes result in an inability of cells to take up glucose.
- Drinking alcoholic beverages leads to an increase in urine output. This most likely occurs because alcohol:
- inhibits ADH release
- stimulates ADH secretion
- inhibits TSH release
- stimulates TSH release
- The release of FSH and LH from the anterior pituitary gland is stimulated by ________.
- What hormone is produced by the beta cells of the pancreas?
- When blood calcium levels are low, PTH stimulates:
- excretion of calcium from the kidneys
- excretion of calcium from the intestine
- Name and describe the function of a hormone produced by the anterior pituitary gland and a hormone produced by the posterior pituitary gland.
- Describe a direct effect of growth hormone (GH).
- In addition to producing FSH and LH, the anterior pituitary gland in women also produces the hormone prolactin (PRL). Prolactin stimulates milk production from the mammary glands after birth. Prolactin levels are regulated by the hypothalamic hormones prolactin-releasing hormone (PRH) and prolactin-inhibiting hormone (PIH), now known as dopamine. PRH stimulates the release of prolactin and PIH inhibits it. The posterior pituitary gland secretes the hormone oxytocin, which stimulates labor during labor. Uterine smooth muscle is not very sensitive to oxytocin until late in pregnancy, when the number of oxytocin receptors in the uterus peaks. Stretching of the tissues in the uterus and vagina stimulates oxytocin release during childbirth. The intensity of labor increases as the level of oxytocin in the blood increases until labor is complete.
- Hormonal regulation is required for the growth and replication of most cells in the body. Growth hormone (GH), produced by the anterior pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bone. Growth hormone has direct and indirect mechanisms of action. Direct effects of GH include: 1) Stimulating the breakdown of fat (lipolysis) and release into the blood by adipocytes. This results in a switch from using glucose as an energy source to using fatty acids in most tissues. This process is called the glucose-sparing effect. 2) In the liver, GH stimulates the breakdown of glycogen, which is then released into the blood as glucose. Blood sugar levels rise because most tissues use fatty acids instead of glucose for their energy needs. The GH-mediated increase in blood sugar levels is called a diabetogenic effect because it is similar to the high blood sugar levels seen in diabetes mellitus.
- Addison's disease
- Disorder caused by hyposecretion of corticosteroids
- Condition caused by overproduction of GH in adults
- Adrenocorticotropes Hormon (ACTH)
- Hormone released by the anterior pituitary gland that stimulates the adrenal cortex to release corticosteroids during the long-term stress response
- Steroid hormone produced by the adrenal cortex that stimulates Na reabsorption+from extracellular fluids and secretion of K+.
- male sex hormone such as testosterone
- Antidiuretisches Hormon (ADH)
- Hormone produced by the hypothalamus and released by the posterior pituitary gland that increases water absorption by the kidneys
- Hormone produced by the parafollicular cells of the thyroid gland that lowers the level of Ca in the blood2+levels and promote bone growth
- Hormone released by the adrenal cortex in response to long-term stress
- Glucocorticoid produced in response to stress
- Morbus Cushing
- Disorder caused by the hypersecretion of glucocorticoids
- Diabetes insipidus
- Disorder caused by underproduction of ADH
- Diabetes Mellitus
- Disorder caused by low insulin activity
- diabetogenic effect
- Effect of GH that raises blood sugar levels similar to diabetes mellitus
- Hormone released by the adrenal medulla in response to short-term stress
- Follicle Stimulating Hormone (FSH)
- Hormone produced by the anterior pituitary gland that stimulates gamete production
- Condition caused by overproduction of GH in children
- Hormone produced by the alpha cells of the pancreas in response to low blood sugar; Functions to increase blood sugar levels
- Corticosteroid that affects glucose metabolism
- Synthesis of glucose from amino acids
- glucose-sparing effect
- Action of GH that causes tissues to use fatty acids instead of glucose as an energy source
- Breakdown of glycogen to glucose
- Enlargement of the thyroid gland caused by insufficient levels of iodine in the diet
- Hormone that regulates the gonads, including FSH and LH
- growth hormone (GH)
- Hormone produced by the anterior pituitary gland that promotes protein synthesis and body growth
- Growth Hormone Inhibitory Hormone (GHIH)
- Hormone produced by the hypothalamus that inhibits growth hormone production, also called somatostatin
- Growth Hormone-Releasing Hormone (GHRH)
- Hormone released by the hypothalamus that triggers the release of GH
- high blood sugar level
- overactive thyroid
- low blood sugar level
- underactive thyroid
- insulin-like growth factor (IGF)
- growth-promoting protein produced by the liver
- Hormone produced by the beta cells of the pancreas in response to high blood sugar levels; Functions to lower blood sugar levels
- Corticosteroid that affects ion and water balance
- Hormone released by the adrenal medulla in response to short-term stress hormone production by the gonads
- Receptor in the hypothalamus that monitors the level of electrolytes in the blood
- Hormone released by the posterior pituitary gland to stimulate uterine contractions during labor and milk secretion in the mammary glands
- Gland on the surface of the thyroid that produces parathyroid hormone
- Parathormon (PTH)
- Hormone produced by the parathyroid glands in response to low levels of Ca in the blood2+levels; Functions to increase blood Ca2+levels
- Pituitary Dwarfism
- Condition caused by underproduction of GH in children
- endocrine gland at the base of the brain, consisting of an anterior and posterior region; also called the pituitary gland
- (also infundibulum) Stalk connecting the pituitary gland to the hypothalamus
- Prolactin (PRL)
- Hormone produced by the anterior pituitary gland that stimulates milk production
- prolactin-inhibiting hormone
- Hormone produced by the hypothalamus that inhibits the release of prolactin
- Hormone produced by the hypothalamus that stimulates the release of prolactin
- Enzyme produced by the juxtaglomerular apparatus of the kidneys that reacts with angiotensinogen to cause release of aldosterone
- Glycoprotein in the thyroid that is converted into thyroid hormone
- endocrine gland in the neck that produces the thyroid hormones thyroxine and triiodothyronine
- Thyroid Stimulating Hormone (TSH)
- Hormone produced by the anterior pituitary gland that stimulates the release of T3and t4from the thyroid
- Thyroxin (Tetraiodthyronin, T4)
- Thyroid hormone that controls the basal metabolic rate
- Trijodthyronin (T3)
- Thyroid hormone that controls the basal metabolic rate