The Endocrine System: Hormones, Glands and Chemical Control
How hormones act, how their release is controlled, and how the pituitary, thyroid, parathyroid, adrenal glands and pancreas maintain homeostasis.
🎯 By the end of this lesson
- Compare nervous and endocrine signalling in medium, speed and duration.
- Classify hormones as amine, peptide or steroid and relate class to receptor location and mechanism.
- Describe the cAMP second-messenger pathway and the intracellular-receptor pathway.
- Distinguish humoral, hormonal and neural stimuli for hormone release and give an example of each.
- Explain how the hypothalamus controls the anterior and posterior pituitary differently.
- Trace the hypothalamus-pituitary-thyroid feedback loop and explain the consequences of iodine deficiency.
- Explain how PTH and calcitonin regulate blood calcium.
- Describe the adrenal cortex and medulla hormones and the stages of the general adaptation syndrome.
- Explain blood glucose regulation by insulin and glucagon and compare type 1 and type 2 diabetes.
1Overview
A person who hears a loud bang jumps within a fraction of a second, yet the shaking hands and pounding heart persist for minutes afterward. The first reaction is nervous; the lingering one is endocrine. The endocrine system is a set of glands and cells that release chemical messengers called hormones into the blood, where they travel to distant targets and change what those cells do. Hormones set the pace of metabolism, regulate blood sugar and calcium, control growth, mediate stress and orchestrate reproduction. This lesson covers how hormones act, how their release is controlled, and the major glands other than the gonads (covered with the reproductive system in Lesson 13).
2Chemical communication: nervous and endocrine compared
The nervous and endocrine systems are the body's two long-distance communicators, and both maintain homeostasis. They differ in medium, speed and precision.
| Feature | Nervous system | Endocrine system |
|---|---|---|
| Signal | electrical and chemical (neurotransmitters) | chemical only (hormones) |
| Route | along neurons; short synaptic gap | through the blood to distant targets |
| Speed | always fast, brief | seconds (adrenal hormones) to hours or up to about 48 hours (some reproductive hormones) |
| Specificity | precise, local | broad; one hormone can affect many cell types in different ways |
| Duration | stops quickly when signalling ends | effects can persist |
Two other kinds of chemical signal act close to their source. Paracrine signals affect neighbouring cells (histamine narrowing airways in asthma) and autocrine signals act on the cell that released them. Hormones are secreted by endocrine glands, which are ductless: the pituitary, thyroid, parathyroid, adrenal and pineal glands release directly into the fluid around their cells, unlike exocrine glands (sweat, sebaceous) that use ducts. Many other organs also contain endocrine cells: the hypothalamus, thymus, heart, kidneys, stomach, small intestine, liver, skin, ovaries and testes, as well as adipose tissue and bone. The pancreas is both an exocrine (digestive) and an endocrine gland.
A hormone reaches every cell it passes, but only target cells respond, because only they have receptors for that hormone. The same hormone can produce different responses in different tissues. Oxytocin, for example, affects uterine contractions, milk release and emotional attachment.
3Hormones: classes and mechanisms of action
| Class | Made from | Examples | Receptor location |
|---|---|---|---|
| Amine | modified amino acids (tryptophan or tyrosine) | melatonin, thyroid hormones, epinephrine | surface (epinephrine, melatonin); intracellular (thyroid hormones) |
| Peptide and protein | chains of amino acids | ADH, growth hormone, insulin | surface of the cell |
| Steroid | cholesterol (lipid-soluble) | cortisol, aldosterone, testosterone, estrogens | inside the cell |
Steroids travel in the blood bound to transport proteins, which lengthens their half-life (cortisol lasts about 60 to 90 minutes), whereas epinephrine lasts about one minute.
Intracellular receptors (steroid and thyroid hormones)
Because they dissolve in lipid, these hormones cross the membrane and bind receptors in the cytosol or nucleus. The hormone-receptor complex attaches to DNA and triggers transcription of a target gene, and the new protein produces the response (Lesson 4). The effect is slower but longer lasting.
Membrane receptors (water-soluble hormones)
Water-soluble hormones cannot cross the bilayer. The hormone is the first messenger; it binds a receptor on the cell surface, and a second messenger carries the message inside. In the cAMP pathway a G protein activates adenylyl cyclase, which converts ATP into cyclic AMP. cAMP activates protein kinases, which phosphorylate proteins in a cascade, and the enzyme phosphodiesterase later breaks cAMP down to end the response. In the calcium pathway a G protein activates phospholipase C, which produces IP3 and releases stored calcium. Each hormone molecule can activate many second messengers, so a tiny concentration of hormone produces a large response (amplification).
Epinephrine binds a receptor on a liver cell. The receptor activates a G protein, adenylyl cyclase makes cAMP, and a kinase cascade converts glycogen to glucose within seconds, so blood glucose rises during fight or flight. In contrast, cortisol enters the same liver cell, binds an internal receptor and switches on genes for gluconeogenesis, a response that takes longer but lasts hours. Both raise glucose, by different mechanisms and on different time scales.
4Control of hormone release
Hormone levels are regulated by three kinds of stimulus.
- Humoral: a change in a blood chemical directly triggers release. Rising blood glucose triggers insulin; rising blood osmolarity triggers ADH.
- Hormonal: one hormone triggers release of another, often through hypothalamic releasing and inhibiting hormones.
- Neural: nerve signals trigger release, as when the sympathetic system stimulates the adrenal medulla to release epinephrine.
Most loops use negative feedback: rising hormone levels inhibit further secretion (Lesson 3). A few use positive feedback with a definite end point, such as oxytocin during childbirth. Target cells also adjust their sensitivity. If a hormone stays high for a long time, the cells may reduce their receptor number (downregulation); if it stays low, receptor number may increase (upregulation). Hormones also interact:
| Interaction | Meaning | Example |
|---|---|---|
| Permissive | one hormone enables another to act | thyroid hormones and reproductive hormones |
| Synergistic | hormones with similar effects amplify each other | FSH and estrogens in egg maturation |
| Antagonistic | hormones oppose one another | insulin lowers blood glucose, glucagon raises it |
5The hypothalamus and pituitary: the command centre
The hypothalamus, in the diencephalon, links the nervous and endocrine systems. It hangs a bean-sized gland, the pituitary, from a stalk. The pituitary has two parts that differ in origin and function.
Posterior pituitary: stores and releases
The posterior pituitary is neural tissue. It does not make hormones; neurosecretory cells in the hypothalamus make ADH and oxytocin, and their axons carry them down to be stored and released into the blood.
- ADH (antidiuretic hormone, vasopressin): osmoreceptors in the hypothalamus detect high blood osmolarity (dehydration, a salty meal) and ADH is released. It acts on kidney tubule cells to increase water reabsorption (Lesson 12). Falling osmolarity lowers ADH, a negative feedback loop. Alcohol inhibits ADH, which increases urine output; chronic ADH deficiency causes diabetes insipidus and chronic dehydration.
- Oxytocin: stimulates uterine contractions and cervical dilation in childbirth (the positive feedback loop of Lesson 3) and the milk let-down reflex during breastfeeding. It is also involved in bonding.
Anterior pituitary: controlled by hypothalamic hormones
The anterior pituitary is glandular tissue that makes its own hormones. The hypothalamus controls it through releasing and inhibiting hormones that travel in a special set of portal vessels directly from the hypothalamus to the anterior pituitary, avoiding the general circulation. TSH, ACTH, FSH and LH are tropic hormones, meaning that they control other endocrine glands.
| Hormone | Target | Main action |
|---|---|---|
| Growth hormone (GH) | bone, muscle, liver, fat | growth and protein synthesis (directly and through IGFs); raises blood glucose; stimulates fat breakdown. Excess in children: gigantism; in adults: acromegaly; deficiency: pituitary dwarfism |
| TSH | thyroid | stimulates thyroid hormone release |
| ACTH | adrenal cortex | stimulates cortisol and other corticosteroids; rises with stress |
| FSH and LH | gonads | gamete production, ovulation and sex hormone release (Lesson 13) |
| Prolactin | mammary glands | milk production |
The pituitary is often called the "master gland". It is better described as the hypothalamus's partner: the hypothalamus decides, and the pituitary executes. The posterior pituitary does not even make the hormones it releases.
6Thyroid, parathyroid and adrenal glands
Thyroid
The butterfly-shaped thyroid lies in front of the trachea. Its follicle cells take up iodide from the blood and attach iodine to a protein (thyroglobulin) stored in the colloid, making T4 (four iodines) and T3 (three iodines, more potent). Thyroid hormones regulate the basal metabolic rate, raising ATP production and oxygen use and releasing heat; they also support growth and nervous-system development and increase sensitivity to epinephrine. The control loop is a classic three-gland negative feedback axis: low T3/T4 makes the hypothalamus release TRH, TRH makes the anterior pituitary release TSH, TSH makes the thyroid release T3/T4, and high T3/T4 suppresses TRH and TSH.
| Condition | Cause | Features |
|---|---|---|
| Iodine deficiency goiter | too little iodine, so T3/T4 are low and TSH stays high | enlarged thyroid; in pregnancy, impaired development of the fetus |
| Hypothyroidism | low thyroid hormone, often from inflammation | low metabolic rate, weight gain, cold intolerance, constipation, reduced mental activity |
| Hyperthyroidism (e.g. Graves disease) | excess hormone; in Graves, autoantibodies overstimulate the thyroid | high metabolic rate, heat intolerance, weight loss, tremor, rapid heart rate, bulging eyes |
Iodine must come from the diet; iodized salt is the main source in many countries, and iodine deficiency is the leading preventable cause of intellectual disability worldwide.
Parathyroid glands and calcium
Calcium is essential for nerve signalling, muscle contraction and clotting, so blood calcium is closely regulated. Usually four small parathyroid glands sit on the back of the thyroid. When blood calcium is low they release parathyroid hormone (PTH), which stimulates osteoclasts to break down bone and release calcium, increases calcium reabsorption in the kidney, and triggers the kidney to make calcitriol, the active form of vitamin D, which increases calcium absorption in the intestine. Rising calcium suppresses PTH (negative feedback). Calcitonin from thyroid C cells opposes PTH when calcium is high, but its physiological role is considered minor.
In real life. If the parathyroid glands are damaged during thyroid surgery, blood calcium falls and nerves and muscles become overexcitable, causing twitching, cramps and spasms; severe cases can paralyze breathing muscles. Too much PTH removes calcium from bone and reduces bone density. Calcium homeostasis therefore protects both the skeleton and the nervous system.
Adrenal glands
The adrenal glands sit on top of the kidneys and have two parts.
| Region | Hormones | Role |
|---|---|---|
| Cortex, outer zone | aldosterone (mineralocorticoid) | sodium retention and potassium excretion; raises blood volume and pressure (RAAS, Lesson 12) |
| Cortex, middle zone | cortisol (glucocorticoid) | breaks down glycogen, fat and protein to supply glucose; suppresses inflammation and immune activity; long-term stress response |
| Cortex, inner zone | androgens | small amounts; converted to testosterone or estrogens |
| Medulla | epinephrine and norepinephrine | fight-or-flight response: higher glucose, heart rate and blood pressure, dilated airways |
The medulla is controlled by the sympathetic nervous system. The cortex is controlled by ACTH through the hypothalamus-pituitary-adrenal (HPA) axis. The general adaptation syndrome describes how the body responds to ongoing stress: an alarm stage driven by the medulla, a resistance stage in which the body adjusts its functions, and, if stress persists, an exhaustion stage driven by cortisol that can bring depression, immune suppression and fatigue. Excess cortisol causes Cushing disease; too little causes Addison disease.
The pineal gland also belongs to the endocrine system: it releases melatonin, an amine hormone linked to the sleep-wake rhythm (see the related article on sleep).
7The endocrine pancreas and blood glucose
The pancreas lies mostly behind the lower stomach. It is mainly an exocrine gland that releases digestive enzymes (Lesson 11), but clusters of endocrine cells called pancreatic islets contain four cell types: alpha cells (about 20%) make glucagon, beta cells (about 75%) make insulin, delta cells make somatostatin (which inhibits both) and PP cells make pancreatic polypeptide.
- Insulin lowers blood glucose. It binds a membrane receptor that moves glucose-transporter vesicles to the surface, so skeletal muscle and fat cells take up glucose by facilitated diffusion (Lesson 3). It also promotes glycolysis, glycogen storage and the synthesis of triglycerides and proteins, and inhibits glycogen breakdown and gluconeogenesis. Gut hormones such as GIP trigger an early rise in insulin after eating.
- Glucagon raises blood glucose. It triggers liver glycogenolysis, gluconeogenesis and the breakdown of fat.
Red blood cells, the brain, liver and kidneys do not need insulin for glucose uptake, which helps keep the brain supplied even when insulin is low. A target range for fasting blood glucose is about 70 to 110 mg/dL (the textbook gives slightly different upper limits in different places).
Diabetes mellitus
| Feature | Type 1 | Type 2 |
|---|---|---|
| Cause | autoimmune destruction of beta cells; genetic susceptibility | insulin resistance of target cells; beta cells eventually become exhausted |
| Insulin | little or none; injection or infusion needed | initially high, later may fall |
| Share of cases | under 5% | about 95% |
| Risk factors | genetic and autoimmune | poor diet, inactivity, overweight (80 to 90% of patients) |
| Management | insulin | weight loss, exercise, diet; medications; insulin if needed |
Symptoms include excessive urination and thirst (glucose in the urine draws water with it, causing dehydration) and persistent hunger. Long-term complications include vascular damage (heart attack, stroke, kidney failure, blindness), nerve damage that increases the risk of injury and infection, and ketoacidosis, in which the liver produces acidic ketone bodies as cells burn fat for fuel; untreated, it can lead to diabetic coma. Type 2 diabetes can often be reversed with moderate weight loss, exercise and a healthy diet (Lesson 14).
A student skips lunch and blood glucose falls to the low end of the range. Alpha cells release glucagon; the liver breaks down glycogen and releases glucose within minutes, and, if fasting continues, makes new glucose from lactate, glycerol and amino acids. After a large sugary snack, glucose rises, beta cells release insulin and muscle, fat and liver take up glucose. The same pancreas runs both halves of the loop, so there is no off switch to forget.
8Interdependence and homeostasis
The endocrine system rarely acts alone. It works with every other system in the body.
| Partner system | Interdependence |
|---|---|
| Nervous | the hypothalamus controls the pituitary; the sympathetic nervous system stimulates the adrenal medulla |
| Cardiovascular | hormones travel in blood; epinephrine, thyroid hormones and aldosterone change heart rate and blood pressure |
| Urinary | ADH and aldosterone control kidney water and salt handling; kidneys make EPO and activate vitamin D |
| Digestive | gut hormones (gastrin, secretin, CCK) coordinate digestion; insulin and glucagon regulate nutrient storage |
| Skeletal | PTH, calcitonin and growth hormone control bone remodelling and growth |
| Reproductive | FSH, LH and sex hormones control gametes and cycles (Lesson 13) |
| Immune | cortisol suppresses inflammation; the thymus is an endocrine organ |
Almost every endocrine loop has the same logic: a sensor detects a variable (glucose, calcium, osmolarity, thyroid hormone), a gland releases a hormone, target cells respond and the response reduces the original stimulus. That is the negative feedback pattern of Lesson 3, applied to chemicals instead of temperature.
🔑Key terms
?Quick check
Try each question first, then reveal the answer.
1. Why can a steroid hormone act inside a cell but a peptide hormone cannot?
Steroid hormones are lipid-soluble and diffuse through the membrane to reach receptors in the cytosol or nucleus. Peptide hormones are water-soluble and cannot cross the lipid bilayer, so they bind surface receptors and use second messengers.
2. Explain how one hormone molecule can produce a large cellular response.
The hormone binds a receptor that activates many G proteins and enzymes, each producing many molecules of second messenger such as cAMP, which activate many kinases. The signal is amplified at each step.
3. Describe how the hypothalamus controls the anterior pituitary and the posterior pituitary.
It controls the anterior pituitary with releasing and inhibiting hormones sent through portal vessels. The posterior pituitary is neural tissue that stores and releases ADH and oxytocin made by hypothalamic neurons whose axons extend into it.
4. A person lives in an area with little dietary iodine and develops an enlarged thyroid. Explain the cause.
Without iodine the thyroid cannot make enough T3 and T4, so negative feedback on the hypothalamus and pituitary is lost and TSH remains high. TSH keeps stimulating the thyroid, which enlarges to form a goiter.
5. Blood calcium falls. Describe the hormonal response.
Parathyroid glands release PTH. It stimulates osteoclasts to release calcium from bone, increases kidney reabsorption of calcium and triggers calcitriol production, which increases intestinal absorption. Blood calcium rises and PTH release falls.
6. Distinguish the roles of the adrenal medulla and the adrenal cortex in stress.
The medulla, under sympathetic control, releases epinephrine and norepinephrine for the rapid fight-or-flight response. The cortex, controlled by ACTH, releases cortisol for the longer-term response and aldosterone for salt and water balance.
7. Explain why people with untreated diabetes urinate frequently and feel very thirsty.
High blood glucose exceeds the kidney's ability to reabsorb it, so glucose appears in the urine and draws water with it by osmosis. The resulting fluid loss causes dehydration and thirst.
8. Compare type 1 and type 2 diabetes in cause and treatment.
Type 1 is caused by autoimmune destruction of beta cells so little insulin is made and insulin must be given. Type 2 involves insulin resistance of target cells and eventual beta cell exhaustion, and it is often managed with weight loss, exercise, diet and medication, with insulin if needed.
BC curriculum content covered in this lesson
- Organ systems: endocrine system (structure and function)
- Structural and functional interdependence (endocrine system with nervous, cardiovascular, urinary, digestive, skeletal and reproductive systems)
- Maintenance of homeostasis (endocrine system: blood glucose, calcium, metabolic rate, stress)
Related articles
How Does the Immune System Work?
The immune system has a fast, general innate layer and a slower, specific adaptive layer with memory. Barriers, white blood cells, antibodies, organs and what happens when it misfires.
Why Sleep Is Not Downtime: What the Brain and Body Do After Dark
Sleep is an active state in which the brain, heart, hormones and immune system all shift gears. US health agencies also publish recommended hours by age, and their figures differ slightly.
Why Does the Body Get a Fever?
A fever is a raised hypothalamic set point triggered by pyrogens, usually during infection. Health sources describe its mechanism, benefits, how it is graded and when care is advised.
References
- OpenStax. Anatomy and Physiology 2e, 17.1 An Overview of the Endocrine System. Accessed October 7, 2026.
- OpenStax. Anatomy and Physiology 2e, 17.2 Hormones. Accessed October 7, 2026.
- OpenStax. Anatomy and Physiology 2e, 17.3 The Pituitary Gland and Hypothalamus. Accessed October 7, 2026.
- OpenStax. Anatomy and Physiology 2e, 17.4 The Thyroid Gland. Accessed October 7, 2026.
- OpenStax. Anatomy and Physiology 2e, 17.5 The Parathyroid Glands. Accessed October 7, 2026.
- OpenStax. Anatomy and Physiology 2e, 17.6 The Adrenal Glands. Accessed October 7, 2026.
- OpenStax. Anatomy and Physiology 2e, 17.9 The Endocrine Pancreas. Accessed October 7, 2026.
- OpenStax. Anatomy and Physiology 2e, 24.1 Overview of Metabolic Reactions. Accessed October 7, 2026.
- BC Ministry of Education and Child Care. Anatomy and Physiology 12 (curriculum). Accessed October 7, 2026.
These lessons follow the content areas listed in the British Columbia curriculum. They are study material written for this site and are not an official document. The official curriculum is the authority on what each course requires. Lessons are general education, not medical advice.