Chemical Co-ordination and Integration | ISC Class 11 Biology Notes
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This note covers chemical messengers, the locations and functions of endocrine glands, hypothalamic and pituitary control, hormone feedback, endocrine disorders, digestive hormones, and the mechanisms of hormone action through cyclic adenosine monophosphate and intracellular receptors.
What are hormones, and where are endocrine glands located?
Definition: Hormones are non-nutrient chemicals produced in trace amounts that carry messages between cells. They coordinate functions such as growth, development and metabolism, the chemical reactions occurring within the body.
Endocrine glands lack ducts, or tubes carrying secretions. Their secretions are hormones. Exocrine glands deliver secretions through ducts. The endocrine system includes both organised glands and hormone-producing cells scattered within other tissues.
Neural coordination provides rapid, short-lived communication between particular points. Nerve fibres do not supply every body cell, while cellular activities require continuous regulation. Hormonal coordination helps meet this need. The neural and endocrine systems jointly coordinate physiological functions, meaning the working activities of the body.
How do location and function fit together?
A target cell responds to a hormone because it has the appropriate receptor, a specific protein that binds that hormone. Blood can transport a hormone to a distant target. The position of a gland and the position of its target therefore need not coincide.
| Endocrine structure | Location in humans | Main association |
|---|---|---|
| Hypothalamus | Basal part of the diencephalon, a forebrain region | Regulation of pituitary hormones |
| Pituitary | In a bony cavity, attached to the hypothalamus by a stalk | Growth and control of several endocrine glands |
| Pineal | Dorsal, or back, side of the forebrain | Daily biological rhythms |
| Thyroid and parathyroids | Thyroid beside the trachea, or windpipe; parathyroids behind the thyroid | Metabolism and calcium regulation |
| Thymus | Between the lungs, behind the sternum, or breastbone | Development of immune responses |
| Adrenals | One above each kidney | Stress responses and regulation of metabolism, water and salts |
| Pancreas | In the abdomen | Blood glucose regulation |
| Gonads, or primary sex organs | Testes in the scrotal sac outside the abdomen; ovaries in the abdomen | Reproductive functions and sexual development |
What the figure shows
Locations of endocrine glands
A human outline shows the hypothalamus, pituitary and pineal in the head; thyroid and parathyroid in the neck; thymus in the chest; and pancreas and adrenals in the abdomen. Separate lower insets identify an ovary in a female and a testis in a male.
See Fig. 19.1 in your NCERT textbook
How does the hypothalamus control the pituitary?
The hypothalamus contains groups of hormone-producing nerve cells. These groups are called nuclei, and the cells are neurosecretory cells. Here, a nucleus means a group of nerve cells, rather than the structure containing genetic material inside an individual cell.
Hypothalamic hormones regulate the synthesis and secretion of pituitary hormones. Releasing hormones stimulate pituitary secretion, whereas inhibiting hormones inhibit it. These two types allow the hypothalamus to regulate rather than merely switch on pituitary activity.
What route do releasing hormones follow?
- Neurosecretory cells in the hypothalamus produce releasing or inhibiting hormones.
- The hormones pass along axons, the processes of nerve cells that conduct signals away from the cell body.
- Nerve endings release the hormones into a portal circulatory system, a blood-vessel connection between two capillary networks.
- This blood supply carries the hormones to the anterior pituitary, where they regulate hormone production and release.
Gonadotrophin-releasing hormone (GnRH) stimulates pituitary synthesis and release of gonadotrophins, hormones that act on the gonads. In contrast, somatostatin inhibits release of growth hormone from the pituitary. These are examples of stimulation and inhibition, respectively.
The posterior pituitary has a different relationship with the hypothalamus. It is under direct neural regulation and receives hormones transported along nerve-cell axons. Its storage and release functions must be distinguished from hormone synthesis in the hypothalamus.
What the figure shows
Hypothalamus and pituitary connection
The drawing labels hypothalamic neurons above the pituitary. It shows portal circulation associated with the anterior pituitary and long neuronal processes extending into the posterior pituitary. Both pituitary regions are labelled.
See Fig. 19.2 in your NCERT textbook
Which hormones are associated with the different pituitary regions?
The pituitary gland lies in a bony cavity called the sella turcica. Its glandular division, the adenohypophysis, contains the pars distalis and pars intermedia. The pars distalis is commonly called the anterior pituitary. In humans, the pars intermedia is almost merged with it.
The neurohypophysis, also called pars nervosa or posterior pituitary, stores and releases oxytocin and vasopressin. Both are actually synthesised in the hypothalamus. Secretion into the blood from the posterior pituitary does not mean production there.
What does each anterior or intermediate hormone do?
| Hormone | Region | Principal action |
|---|---|---|
| Growth hormone (GH) | Pars distalis | Promotes body growth |
| Prolactin (PRL) | Pars distalis | Regulates mammary (milk-producing) gland growth and milk formation |
| Thyroid-stimulating hormone (TSH) | Pars distalis | Stimulates thyroid hormone synthesis and secretion |
| Adrenocorticotrophic hormone (ACTH) | Pars distalis | Stimulates glucocorticoid secretion from the adrenal cortex, the outer adrenal tissue; glucocorticoids are hormones regulating carbohydrate metabolism |
| Luteinising hormone (LH) | Pars distalis | Stimulates testicular androgen production; in females induces ovulation and maintains the corpus luteum |
| Follicle-stimulating hormone (FSH) | Pars distalis | With androgens regulates sperm formation in males; stimulates ovarian follicle growth in females |
| Melanocyte-stimulating hormone (MSH) | Pars intermedia | Acts on melanocytes, the pigment-containing cells, to regulate skin pigmentation |
Androgens are male sex hormones. An ovarian follicle is the ovarian structure containing a developing egg. Ovulation is the release of the egg from a mature follicle. The corpus luteum is the structure formed from the follicle's remnants afterwards.
How do growth hormone disturbances affect the body?
Hyposecretion means reduced hormone secretion; hypersecretion means excessive secretion. Low GH secretion during growth produces pituitary dwarfism, with stunted growth. Excess GH during growth produces gigantism, with abnormal overgrowth of the body.
Excess GH in adults, especially in middle age, can cause acromegaly, severe disfigurement especially affecting the face. It may cause serious complications if unchecked. Early diagnosis is difficult, and the condition often goes undetected for many years until external changes become noticeable.
How do oxytocin and vasopressin act?
Oxytocin stimulates contraction of smooth muscle, the involuntary muscle of internal organs. It causes vigorous uterine contractions during childbirth and milk ejection from mammary glands. Prolactin promotes milk formation; oxytocin promotes its ejection.
Vasopressin, or antidiuretic hormone (ADH), acts mainly on the kidneys. It promotes reabsorption of water and electrolytes, dissolved substances yielding ions, by distal kidney tubules. Reabsorption returns substances from the forming urine to the blood and reduces diuresis, or urinary water loss.
Impaired ADH synthesis or release reduces the kidneys' ability to conserve water. The resulting water loss and dehydration, meaning depletion of body water, characterise diabetes insipidus.
How does feedback regulate tropic hormones?
A tropic hormone stimulates another endocrine gland. TSH acts on the thyroid, and ACTH acts on the adrenal cortex. These relationships place the pituitary between hypothalamic signals and the hormone output of a peripheral endocrine gland, meaning one outside the hypothalamus and pituitary.
Negative feedback occurs when an increase in a pathway's final output reduces the signals promoting that output. Hormone concentration therefore influences further secretion. This helps maintain homeostasis, the regulation of internal conditions within suitable limits.
How does thyroid feedback work?
- The hypothalamus releases thyrotrophin-releasing hormone (TRH), which stimulates TSH secretion from the anterior pituitary.
- TSH stimulates the thyroid to synthesise and release thyroid hormones.
- Rising thyroid hormone levels inhibit further TRH and TSH secretion through negative feedback.
- When thyroid hormone levels fall, this inhibition decreases, allowing stimulation of the thyroid to increase.
What is another example?
The hypothalamus releases corticotrophin-releasing hormone (CRH), which promotes ACTH secretion. ACTH stimulates the adrenal cortex to produce cortisol, its main glucocorticoid. Rising cortisol feeds back to reduce CRH and ACTH secretion. Falling cortisol reduces this inhibition.
Note: A tropic hormone and a target-gland hormone are different signals. TSH stimulates the thyroid; thyroid hormones then act on body tissues and participate in feedback. Feedback describes regulation of secretion, rather than transport of the hormone back to its gland.
How do the pineal gland and thymus support body regulation?
What does melatonin regulate?
The pineal gland, on the dorsal side of the forebrain, secretes melatonin. It helps regulate the body's diurnal rhythm, the pattern repeating over approximately a day. The rhythm described here is a 24-hour rhythm.
Melatonin helps maintain normal sleep-wake and body-temperature rhythms. It also influences metabolism, pigmentation, the menstrual cycle and the body's defence capability. Thus its actions extend beyond sleep, although sleep-wake timing is a useful example of its daily regulatory role.
Why is the thymus associated with immunity?
The thymus is a lobular gland between the lungs, behind the sternum and in front of the aorta, the main artery leaving the heart. It secretes thymosins, peptide hormones. Peptides are chains of amino acids, the building units of proteins.
Thymosins help the differentiation of T-lymphocytes, immune cells that provide cell-mediated immunity. Differentiation is the development of specialised cellular characteristics. Cell-mediated immunity depends on immune cells acting against targets rather than on antibodies alone.
Thymosins also promote production of antibodies, proteins involved in recognising particular foreign substances. This supports humoral immunity, immunity mediated by antibodies in body fluids. Both actions should be included when explaining thymosin function.
The thymus degenerates in old individuals, reducing thymosin production and contributing to weaker immune responses. The connection is between a change in gland activity, reduced hormone output and reduced immune function. It is distinct from melatonin's regulation of daily rhythms.
How do thyroid hormones act, and what happens when their secretion changes?
The thyroid has two lobes, one on each side of the trachea, joined by an isthmus, a thin connective-tissue bridge. Its follicles are small structures whose follicular cells surround a cavity. These cells synthesise the iodine-containing thyroid hormones.
Thyroxine, also called tetraiodothyronine, is abbreviated T₄; triiodothyronine is abbreviated T₃. The subscripts indicate four and three iodine atoms, respectively. Iodine is essential for the normal rate of their synthesis.
What are the normal actions?
Thyroid hormones regulate the basal metabolic rate, the body's rate of energy use under basal resting conditions. They control carbohydrate, protein and fat metabolism, support red blood cell formation, influence water and electrolyte balance, and contribute to normal development.
The thyroid also secretes thyrocalcitonin (TCT), a protein hormone that lowers blood calcium. TCT must be distinguished from T₃ and T₄: sharing a gland of origin does not give hormones identical functions.
How do deficiency and excess differ?
Hypothyroidism means deficient thyroid hormone activity. Dietary iodine deficiency causes hypothyroidism and thyroid enlargement, termed goitre. Hypothyroidism during pregnancy impairs the growing baby's development and maturation, producing the developmental disorder called cretinism.
Cretinism involves stunted growth and impaired intellectual development; abnormal skin and impaired hearing and speech can also occur. In adult women, hypothyroidism may make the menstrual cycle irregular. The qualification “may” matters: this is not an inevitable effect in every individual.
Hyperthyroidism is excessive thyroid hormone activity. Thyroid cancer or the development of nodules, localised lumps in the gland, increase hormone synthesis and secretion to abnormally high levels, adversely affecting body functions.
Exophthalmic goitre, also called Graves' disease, is a form of hyperthyroidism. Its characteristic features include thyroid enlargement, protruding eyeballs, increased basal metabolic rate and weight loss. Goitre describes enlargement; the word alone does not specify whether thyroid hormone levels are low or high.
What the figure shows
Thyroid and parathyroid positions
The ventral, or front, view shows the thyroid beside the trachea and labels the vocal cord. The dorsal view shows the parathyroid glands as small structures on the back of the thyroid lobes.
See Fig. 19.3 in your NCERT textbook
How do the parathyroids regulate calcium balance?
Humans have four parathyroid glands on the back of the thyroid, with one pair associated with each thyroid lobe. They secrete parathyroid hormone (PTH), a peptide hormone. Circulating calcium levels regulate its secretion.
The symbol Ca²⁺ denotes a calcium ion carrying two positive charges. PTH raises blood Ca²⁺ and is therefore called hypercalcaemic. Calcium balance is an example of homeostasis involving coordinated changes in several organs.
Which organs respond to PTH?
- Bones: PTH stimulates bone resorption, the dissolution or removal of bone mineral, releasing calcium into the blood.
- Kidneys: PTH stimulates calcium reabsorption by renal tubules, the kidney tubes through which forming urine passes.
- Digestive tract: PTH increases absorption of calcium from digested food into the body.
These effects increase the calcium available in blood. Thyrocalcitonin acts in the opposite direction by lowering blood calcium. PTH and TCT therefore contribute together to calcium balance, although they originate from different glands.
What can disturbed secretion cause?
Too little PTH can lower blood calcium and cause tetany, repeated involuntary muscle spasms associated with increased neuromuscular excitability. Excess PTH can promote excessive loss of bone mineral, weakening bones while increasing blood calcium.
Do not confuse calcium regulation with blood glucose regulation. PTH is hypercalcaemic because it raises calcium; glucagon is hyperglycaemic because it raises glucose. The similar prefixes describe an increase, but the substances being regulated differ.
How do the adrenal cortex and medulla differ?
Each adrenal gland lies above a kidney. Its central tissue is the adrenal medulla; the surrounding tissue is the adrenal cortex. The cortex has an outer zona glomerulosa, middle zona fasciculata and inner zona reticularis, the names of its three tissue layers.
What happens during an emergency response?
The medulla produces adrenaline, or epinephrine, and noradrenaline, or norepinephrine. Together these hormones are called catecholamines. They are rapidly secreted in stress and emergencies and are known as fight-or-flight hormones.
They increase alertness, pupil dilation, sweating and piloerection, meaning raising of body hairs. They also increase heart rate, the strength of heart contraction and breathing rate. Breakdown of glycogen, the stored form of glucose, increases blood glucose; lipid and protein breakdown also increase.
Which hormones come from the cortex?
| Hormone or group | Region | Major action |
|---|---|---|
| Adrenaline | Medulla | Rapid emergency responses and increased fuel availability |
| Noradrenaline | Medulla | Increased alertness and cardiovascular and respiratory activity |
| Cortisol, the main glucocorticoid | Cortex | Regulates metabolism and suppresses inflammatory and immune responses |
| Aldosterone, the main mineralocorticoid | Cortex | Regulates water and electrolyte balance through the kidneys |
| Small amounts of androgenic steroids | Cortex | Contribute to pubic, facial and armpit hair growth at puberty |
Glucocorticoids stimulate gluconeogenesis, formation of glucose from non-carbohydrate materials; lipolysis, lipid breakdown; and proteolysis, protein breakdown. They inhibit cellular uptake and use of amino acids. Cortisol also supports cardiovascular and kidney functions and stimulates red blood cell production.
Mineralocorticoids regulate water and electrolytes. Aldosterone acts mainly on renal tubules, increasing reabsorption of sodium ions, written Na⁺, and water, while increasing excretion of potassium ions, written K⁺, and phosphate ions. Each plus sign denotes one positive charge.
These actions help maintain body fluid volume, blood pressure and osmotic pressure, pressure associated with dissolved substances drawing water across a selectively permeable membrane. Such a membrane allows some substances to cross more readily than others.
What are the effects of abnormal cortical secretion?
Underproduction of adrenal cortical hormones disturbs carbohydrate metabolism and causes acute weakness and fatigue in Addison's disease. Excess cortisol can produce Cushing's syndrome, associated with raised blood glucose, muscle weakness and abnormal fat distribution.
Excess aldosterone can increase sodium and water retention, raise blood pressure and increase potassium loss. Deficiency can cause sodium and water loss and impair potassium excretion. These effects follow from aldosterone's normal renal actions.
What the figure shows
Adrenal gland structure
One drawing shows an adrenal gland above a kidney. An enlarged section labels the outer adrenal cortex and inner adrenal medulla. The figure distinguishes location from internal organisation.
See Fig. 19.4 in your NCERT textbook
How do insulin and glucagon maintain blood glucose?
The pancreas is a composite gland with endocrine and exocrine functions. Its hormone-producing regions are the Islets of Langerhans. A normal human pancreas contains about 1 to 2 million islets, representing only 1 to 2 per cent of pancreatic tissue.
The two main islet cell types are α-cells, pronounced alpha cells, which secrete glucagon, and β-cells, pronounced beta cells, which secrete insulin. Both hormones are peptides, but their effects on blood glucose differ.
How do their actions compare?
| Feature | Glucagon | Insulin |
|---|---|---|
| Cell of origin | Alpha cells of pancreatic islets | Beta cells of pancreatic islets |
| Main target cells described | Hepatocytes, meaning liver cells | Hepatocytes and adipocytes, meaning fat-storage cells |
| Effect on cellular glucose use | Reduces uptake and utilisation | Enhances uptake and utilisation |
| Effect on glycogen | Stimulates glycogenolysis, the breakdown of glycogen | Stimulates glycogenesis, the formation of glycogen from glucose |
| Blood glucose effect | Raises glucose; hyperglycaemic | Lowers glucose; hypoglycaemic |
Glucagon also stimulates gluconeogenesis, further increasing blood glucose. Insulin promotes rapid movement of glucose from blood into its target cells. Together, insulin and glucagon maintain glucose homeostasis through their opposing actions.
How does diabetes mellitus differ from diabetes insipidus?
Diabetes mellitus can result from insulin deficiency and/or insulin resistance, a reduced response of target tissues to insulin. Prolonged hyperglycaemia, meaning raised blood glucose, is associated with glucose loss in urine and formation of harmful compounds called ketone bodies.
Diabetes insipidus concerns failure to conserve water when ADH synthesis or release is impaired. Its mechanism differs from insulin-related glucose imbalance. The shared word “diabetes” does not identify the hormone involved.
Excess insulin can produce hypoglycaemia, abnormally low blood glucose. When revising an endocrine disorder, connect the gland, hormone and direction of change to the resulting disturbance, rather than memorising the disease name alone.
How do gonadal hormones regulate reproduction and development?
What are the endocrine functions of the testes?
The testes produce sperm and also act as endocrine glands. They contain seminiferous tubules, the tubes involved in sperm production, and interstitial tissue between the tubules. Leydig cells, or interstitial cells, secrete androgens, mainly testosterone.
Testosterone supports development, maturation and function of male accessory reproductive organs. Androgens stimulate muscular growth, facial and armpit hair, and a low-pitched voice. They promote spermatogenesis, the formation of spermatozoa, or sperm cells, and influence male sexual behaviour.
Androgens have anabolic effects, meaning effects favouring synthesis of body substances, on protein and carbohydrate metabolism. LH stimulates androgen secretion, while FSH and androgens regulate spermatogenesis. Thus pituitary and testicular hormones cooperate in reproductive function.
What are the endocrine functions of the ovaries?
The ovaries produce eggs and the steroid hormones oestrogens and progesterone. Steroid hormones belong to a group of lipid-derived hormones. Oestrogens are secreted mainly by growing follicles; the corpus luteum formed after ovulation secretes mainly progesterone.
Oestrogens stimulate growth and activity of female reproductive organs, follicle development, female secondary sexual characteristics and mammary gland development. Secondary sexual characteristics are sex-related features developing at puberty beyond the primary reproductive organs.
Progesterone supports pregnancy. In mammary glands, it promotes formation of alveoli, sac-like structures that store milk, and milk secretion. Its pregnancy-supporting function should be distinguished from oxytocin's stimulation of uterine contraction during childbirth.
Deficient gonadal hormone secretion before puberty can delay sexual maturation; excessive secretion before the usual age can cause early appearance of sexual characteristics. Reduced secretion in adults can impair reproductive function. These effects depend on which hormone is affected and the person's developmental stage.
Which hormones are secreted by the gastrointestinal tract?
The gastrointestinal tract (GI tract) is the digestive passage including the stomach and intestines. Endocrine cells within its walls produce hormones that coordinate digestive secretions and movement. Hormone production is therefore not restricted to separate, conspicuous endocrine glands.
Which signal acts on which target?
| Hormone | Target | Action |
|---|---|---|
| Gastrin | Gastric glands in the stomach | Stimulates secretion of hydrochloric acid and pepsinogen |
| Secretin | Exocrine pancreas | Stimulates secretion of water and bicarbonate ions |
| Cholecystokinin-pancreozymin (CCK-PZ), also called cholecystokinin (CCK) | Pancreas and gall bladder | Stimulates pancreatic enzyme secretion and release of bile, respectively |
| Gastric inhibitory peptide (GIP) | Stomach | Inhibits gastric secretion and motility |
Pepsinogen is the inactive precursor of pepsin, an enzyme that digests proteins. An enzyme is a biological catalyst that speeds a reaction. Bicarbonate ions help provide an alkaline, acid-neutralising component of pancreatic secretion.
Bile is the digestive fluid made by the liver and stored in the gall bladder. Distinguish release of stored bile from its production: CCK promotes discharge from the gall bladder. Motility means movement produced by contractions of the digestive tract.
The four hormones coordinate different components of digestion. Gastrin promotes gastric secretion; secretin stimulates the water and bicarbonate component of pancreatic secretion; CCK promotes pancreatic enzymes and bile release; GIP inhibits gastric secretion and movement. Their targets explain why their effects are complementary.
These signals are peptide hormones. Their action illustrates chemical coordination between different digestive structures: a hormone-producing cell signals to a target whose response changes digestive activity. Knowing both the target and its response gives a fuller explanation than naming the hormone alone.
How do cyclic adenosine monophosphate (cAMP) and steroid hormone mechanisms differ?
Hormones act by binding to specific receptors and forming a hormone-receptor complex. Some receptors are membrane-bound, on the cell surface; others are intracellular, inside the target cell, mostly in the nucleus. Binding initiates biochemical changes that alter cell function.
How does the cAMP pathway transmit a signal?
Cyclic adenosine monophosphate (cAMP) is an intracellular second messenger, a molecule that passes on the signal initiated by a hormone. The hormone is the first messenger. Hormones acting through membrane-bound receptors normally do not enter the target cell.
- The hormone binds to its specific receptor on the outer surface of the target-cell membrane.
- The activated receptor signals through a G protein, a membrane-associated signal-relaying protein, to activate the enzyme adenylyl cyclase.
- Adenylyl cyclase converts adenosine triphosphate (ATP), a cellular energy-transfer molecule, into cAMP.
- cAMP activates protein kinases, enzymes that add phosphate groups to proteins and change their activity.
- Changes in protein and enzyme activity alter cellular metabolism and produce the physiological response.
This is the cAMP route, not a claim that every membrane-bound hormone receptor uses cAMP. The important distinction is that an extracellular hormone can trigger an intracellular response through a second messenger.
What the figure shows
Membrane receptor action
FSH is shown binding to a receptor on an ovarian cell membrane. Arrows lead to second-messenger generation, biochemical responses and a physiological response exemplified by ovarian growth.
See Fig. 19.5a in your NCERT textbook
How does a steroid hormone act?
Steroid hormones, such as cortisol, testosterone and progesterone, interact with intracellular receptors. Such hormones mostly regulate gene expression, the use of genetic information to produce cellular products. Their hormone-receptor complexes interact with the genome, the cell's genetic material.
- The steroid hormone enters the target cell through its membrane.
- It binds to an intracellular receptor, forming a hormone-receptor complex.
- The complex interacts with genetic material in the nucleus and changes gene expression.
- Messenger ribonucleic acid (mRNA), which carries genetic instructions for protein synthesis, is produced, and proteins are synthesised.
- The resulting biochemical changes produce physiological and developmental effects, including growth and differentiation.
What the figure shows
Steroid hormone action
Oestrogen is shown entering through a uterine cell membrane. The diagram identifies a hormone-receptor complex in the nucleus and links the genome to mRNA, proteins, and tissue growth and differentiation.
See Fig. 19.5b in your NCERT textbook
The mechanisms differ in receptor location and how the signal reaches cellular machinery. The cAMP route changes protein activity through a second messenger; the steroid route mostly changes gene expression. Both begin with specific hormone recognition and end in altered target-cell function.
Glossary
- Hormone — A non-nutrient chemical produced in trace amounts that carries messages between cells.
- Endocrine gland — A ductless gland whose secretions are hormones involved in regulating body functions.
- Target cell — A cell with a suitable receptor through which a particular hormone produces its effects.
- Neurosecretory cell — A specialised nerve cell that produces and releases hormones for chemical coordination.
- Tropic hormone — A hormone that stimulates another endocrine gland to produce and secrete its hormones.
- Negative feedback — Regulation in which increasing output reduces the signals that stimulate further output.
- Homeostasis — Regulation of internal conditions within suitable limits through coordinated physiological responses.
- Hyposecretion — Reduced secretion of a hormone, potentially causing deficiency of its normal effects.
- Hypersecretion — Excessive secretion of a hormone, potentially exaggerating or disturbing its normal effects.
- Glycogenolysis — Breakdown of stored glycogen, contributing to increased glucose availability in the body.
- Glycogenesis — Formation of glycogen from glucose, promoted by insulin in its target cells.
- Gluconeogenesis — Formation of glucose from non-carbohydrate materials, stimulated by glucagon and glucocorticoids.
- Second messenger — An intracellular signalling molecule that relays a signal initiated at a membrane receptor.
- Hormone-receptor complex — The combination formed when a hormone binds to its specific receptor protein.
Common errors and misconceptions
- Misconception: The posterior pituitary synthesises oxytocin and ADH. Correct: These hormones are synthesised in the hypothalamus, transported along axons, and stored and released by the posterior pituitary.
- Misconception: Prolactin and oxytocin perform the same milk-related function. Correct: Prolactin regulates milk formation, while oxytocin stimulates milk ejection from the mammary glands.
- Misconception: All goitre indicates low thyroid hormone levels. Correct: Goitre means thyroid enlargement; iodine-deficiency goitre is associated with hypothyroidism, whereas exophthalmic goitre is a form of hyperthyroidism.
- Misconception: Diabetes mellitus and diabetes insipidus have the same hormonal cause. Correct: Mellitus involves insulin deficiency and/or resistance; impaired ADH synthesis or release can cause insipidus through reduced water conservation.
- Misconception: The adrenal medulla secretes cortisol. Correct: Cortisol comes from the cortex. The medulla secretes adrenaline and noradrenaline, the rapidly released emergency hormones.
- Misconception: PTH lowers blood calcium while insulin raises blood glucose. Correct: PTH raises blood calcium; insulin lowers blood glucose by promoting uptake, utilisation and glycogen formation.
- Misconception: Every hormone must enter its target cell. Correct: Hormones acting through membrane-bound receptors normally remain outside; intracellular second messengers relay their signal.
- Misconception: CCK causes the gall bladder to manufacture bile. Correct: The gall bladder stores and releases bile; the liver produces it. CCK promotes its release.
Exam-style questions with model answers
Q1. Define a hormone and explain why an endocrine gland is called ductless. [2 marks]
- A hormone is a non-nutrient chemical, produced in trace amounts, that carries messages between cells.
- An endocrine gland is called ductless because it lacks a duct for carrying its hormone secretion.
Q2. Explain three aspects of hypothalamic control: the action of GnRH, the action of somatostatin, and the route by which these hormones reach the anterior pituitary. [3 marks]
- Gonadotrophin-releasing hormone, or GnRH, stimulates the anterior pituitary to synthesise and release gonadotrophins, which regulate gonadal activity.
- Somatostatin has an inhibitory action: it suppresses the release of growth hormone from the pituitary.
- These hypothalamic hormones pass along neuronal axons, leave nerve endings and reach the anterior pituitary through a portal circulatory system.
Q3. State the hormonal disturbance and principal effect in each of these conditions: pituitary dwarfism, acromegaly, exophthalmic goitre and Addison's disease. [4 marks]
- Pituitary dwarfism results from low growth hormone secretion during growth, producing stunted growth of the body.
- Acromegaly can result from excess growth hormone in adults, causing severe disfigurement, especially of the face.
- Exophthalmic goitre involves hyperthyroidism, with thyroid enlargement, protruding eyeballs, increased basal metabolic rate and weight loss.
- Addison's disease involves underproduction of adrenal cortical hormones, disturbed carbohydrate metabolism, and acute weakness and fatigue.
Q4. Compare insulin and glucagon under five headings: cells of origin, chemical nature, main target cells, metabolic actions, and effects on blood glucose. [5 marks]
- Insulin is secreted by beta cells of the pancreatic Islets of Langerhans, whereas glucagon is secreted by their alpha cells.
- Both insulin and glucagon are peptide hormones. Their shared chemical category does not mean that they produce identical metabolic effects.
- Insulin acts mainly on hepatocytes and adipocytes, meaning liver cells and fat-storage cells. Glucagon acts mainly on hepatocytes.
- Insulin promotes glucose uptake, utilisation and glycogenesis. Glucagon promotes glycogenolysis and gluconeogenesis and reduces cellular glucose uptake and utilisation.
- Insulin lowers blood glucose and is hypoglycaemic; glucagon raises it and is hyperglycaemic. Together their actions maintain blood glucose homeostasis.
Q5. Explain thyroid negative feedback in five steps, covering the hypothalamic signal, pituitary signal, thyroid response, response to rising thyroid hormones, and response to falling thyroid hormones. [5 marks]
- The hypothalamus releases thyrotrophin-releasing hormone, abbreviated TRH. This signal reaches the anterior pituitary and stimulates its secretion of thyroid-stimulating hormone.
- The anterior pituitary releases thyroid-stimulating hormone, or TSH. TSH is a tropic hormone because its target is another endocrine gland.
- TSH stimulates the thyroid gland to synthesise and secrete thyroid hormones, which enter the blood and act on target tissues.
- As thyroid hormone levels rise, they inhibit further TRH and TSH secretion. This reduces the stimulation driving further thyroid hormone output.
- As thyroid hormone levels fall, this inhibition decreases, allowing increased stimulation of the thyroid. The feedback therefore opposes the original change.
Q6. Contrast the cAMP pathway with steroid hormone action in six points: membrane-pathway receptor location, cAMP generation, cAMP action, steroid entry and binding, steroid effects on gene expression, and the resulting cellular response. [6 marks]
- In the cAMP pathway, a hormone binds to a membrane-bound receptor and normally does not enter the target cell itself.
- Receptor signalling through a G protein activates adenylyl cyclase, which converts ATP into cyclic adenosine monophosphate, the second messenger cAMP.
- cAMP activates protein kinases. These enzymes add phosphate groups to proteins, changing their activity and thereby altering cellular metabolism.
- A steroid hormone enters the target cell and binds to an intracellular receptor, forming a hormone-receptor complex within the cell.
- The steroid hormone-receptor complex interacts with genetic material and mostly regulates gene expression, leading to messenger RNA production and protein synthesis.
- Both pathways alter target-cell function. The cAMP pathway changes protein activity through signalling; steroid action produces biochemical changes through altered gene expression.
Q7. Name the target and action of each digestive hormone: gastrin, secretin, CCK-PZ and GIP. [4 marks]
- Gastrin acts on the gastric glands in the stomach and stimulates their secretion of hydrochloric acid and pepsinogen.
- Secretin acts on the exocrine pancreas and stimulates the secretion of water and bicarbonate ions.
- Cholecystokinin-pancreozymin, or CCK-PZ, acts on the pancreas and gall bladder, promoting pancreatic enzyme secretion and bile release, respectively.
- Gastric inhibitory peptide, or GIP, acts on the stomach to inhibit gastric secretion and motility, meaning muscular movement.
Q8. In a simplified case, ADH synthesis or release is impaired. ADH normally promotes kidney water reabsorption. Predict the change in urinary water loss, the consequence for body water, and the name of the resulting condition. [3 marks]
- Reduced ADH action decreases the kidneys' ability to reabsorb water, so more water is lost through urine than would otherwise be conserved.
- Increased urinary water loss reduces the body's water reserve and can produce dehydration, meaning depletion of body water.
- The condition caused by impaired ADH synthesis or release and reduced kidney water conservation is called diabetes insipidus.
Key takeaways
- Hormones are trace chemical messengers; their effects depend on specific receptors in target cells and tissues.
- The hypothalamus regulates anterior pituitary secretion and synthesises the oxytocin and ADH released from the posterior pituitary.
- Negative feedback links target-gland hormone output to hypothalamic and pituitary signals, helping regulate further hormone secretion.
- Thyroid hormones regulate metabolism and development; thyroid enlargement can occur with either deficient or excessive thyroid hormone activity.
- PTH raises blood calcium through effects on bones, kidneys and intestinal absorption, while thyrocalcitonin lowers blood calcium.
- The adrenal medulla produces emergency hormones, while the cortex produces glucocorticoids, mineralocorticoids and small amounts of androgenic steroids.
- Insulin lowers blood glucose and glucagon raises it; diabetes mellitus and diabetes insipidus involve different hormonal mechanisms.
- Membrane-bound receptor pathways can use cAMP, while steroid hormone-receptor complexes mostly regulate gene expression inside target cells.
Test yourself
Where are oxytocin and ADH synthesised, and where are they released?
Both are synthesised in the hypothalamus, transported along axons, and stored and released by the posterior pituitary.
Which hormone regulates skin pigmentation through melanocytes?
Melanocyte-stimulating hormone, secreted by the pars intermedia of the pituitary, acts on melanocytes to regulate skin pigmentation.
Which pineal hormone influences daily rhythms?
Melatonin helps regulate the 24-hour rhythm, including normal sleep-wake and body-temperature rhythms.
Why can the thymus be linked to both forms of immunity?
Thymosins support T-lymphocyte differentiation for cell-mediated immunity and promote antibody production for humoral immunity.
What are the main glucocorticoid and mineralocorticoid in humans?
Cortisol is the main glucocorticoid, and aldosterone is the main mineralocorticoid; both are secreted by the adrenal cortex.
Which pancreatic cells secrete glucagon and insulin?
Alpha cells of the Islets of Langerhans secrete glucagon, while beta cells secrete insulin.
What does the corpus luteum mainly secrete?
The corpus luteum mainly secretes progesterone, a steroid hormone that supports pregnancy and influences mammary gland development.
What is the role of cAMP in hormone action?
cAMP acts inside the target cell as a second messenger, relaying a membrane-receptor signal to protein kinases and cellular responses.
