Jugami Biology

Biology · Lesson 17

Homeostasis and Hormones

After a meal, blood glucose climbs. Insulin rises to meet it, and both settle back. That quiet correction is homeostasis at work.

This lesson looks closely at the feedback loops that hold the body steady, and at the hormones that carry many of their messages.

A line chart of the blood-glucose model after a big meal in a typical body. Glucose rises, insulin rises with it, and both fall back as glucose returns to the set point.

1. Keeping steady

Homeostasis is keeping the inside of the body within a narrow range, whatever happens outside. Cells, tissues and organs die if the fluid around them drifts too far (see Libretti and Puckett).

The idea is old. In 1865 Claude Bernard wrote of a milieu intérieur, an internal environment, and in 1926 Walter Cannon named the process homeostasis, from Greek words for “similar” and “standing still” (see Libretti and Puckett). The value the body aims for is its set point.

The Human Body lesson gives a first look at homeostasis. This lesson goes further into the loops and the hormones behind them.

2. Control loops and feedback

Every homeostatic loop has three working parts:

Negative feedback reverses the change, so the variable swings back toward the set point. Many hormones are controlled this way: a gland senses the level of the substance it regulates (see SEER).

Positive feedback pushes the change further, so it builds until some event ends it. In labour, contractions of the womb trigger the release of oxytocin, which causes more contractions, which release more oxytocin. The loop stops once the baby is born (see You and Your Hormones). Blood clotting works in a similar way: thrombin, a key clotting enzyme, speeds up its own production through positive feedback loops (see Zavyalova and others), so a clot forms fast.

3. Temperature

A healthy core temperature is 37 ± 0.5 °C. The body's thermostat is in the preoptic area of the hypothalamus. Thermoreceptors in the skin sense surface temperature, and others in the spinal cord, the organs and the hypothalamus itself sense core temperature (see Osilla and others).

When the body is too warm, blood vessels in the skin widen, called vasodilation, and sweat glands release sweat. When it is too cold, the vessels narrow, called vasoconstriction, skeletal muscles shiver, and body hair stands up (see Tansey and Johnson). Behaviour helps too, like taking off a coat.

Explore: step through the body's thermostat

The control loop: stimulus, receptors, control center, effectors, and the response feeding back.StimulusReceptorsControl centerEffectorsResponsefeeds back

Turn on JavaScript to step through the loop. Here are both versions:

Too hot

  1. Stimulus: core temperature rises above about 37 °C, after exercise on a hot day.
  2. Receptors: thermoreceptors in the skin and inside the body detect the rise and signal the hypothalamus.
  3. Control center: the hypothalamus compares the reading with its set point and sends out signals to cool down.
  4. Effectors: sweat glands release sweat, and blood vessels in the skin widen, called vasodilation.
  5. Response: sweat evaporates and warm blood near the skin loses heat, so temperature falls back toward the set point. The fall switches the response off: negative feedback.

Too cold

  1. Stimulus: core temperature drops below about 37 °C, on a cold night.
  2. Receptors: thermoreceptors in the skin and inside the body detect the drop and signal the hypothalamus.
  3. Control center: the hypothalamus compares the reading with its set point and sends out signals to warm up.
  4. Effectors: skeletal muscles shiver, and blood vessels in the skin narrow, called vasoconstriction.
  5. Response: shivering makes heat and less warm blood reaches the skin, so temperature rises back toward the set point. The rise switches the response off: negative feedback.

Adapted from the descriptions in Osilla and others and Tansey and Johnson.

4. Blood glucose and diabetes

The pancreas has clusters of cells called the islets of Langerhans. Beta cells there release insulin when blood glucose is high, and alpha cells release glucagon when it is low (see SEER).

Insulin lets muscle, liver and fat cells take glucose up from the blood. As glucose falls back to normal, insulin release slows (see You and Your Hormones). Glucagon works the opposite way. It acts on the liver, which breaks down its glycogen store into glucose and also makes new glucose (see You and Your Hormones).

Explore: the blood-glucose feedback model

The model after a big meal in a typical body: glucose rises then returns to the set point as insulin rises and falls.SetGlucoseInsulinGlucagon, dashed0 h1 h2 h3 h4 hA model, not real data

Turn on JavaScript to change the meal and the body. What the model shows for each case:

  • A big meal, a typical body. Glucose peaks at 134 model units and is at 101 after 4 hours, against a set point of 100. Insulin rises with glucose, then falls as glucose returns: negative feedback.
  • A big meal, type 1 diabetes, untreated. Glucose starts high at 150 model units, peaks at 215 model units and is at 207 after 4 hours, against a set point of 100. No insulin is made, so the feedback loop is broken and glucose stays high.
  • A big meal, type 2 diabetes. Glucose peaks at 149 model units and is at 120 after 4 hours, against a set point of 100. Insulin is made, but cells respond weakly to it, so glucose falls slowly.
  • A small snack, a typical body. Glucose peaks at 114 model units and is at 100 after 4 hours, against a set point of 100. Insulin rises with glucose, then falls as glucose returns: negative feedback.
  • A small snack, type 1 diabetes, untreated. Glucose starts high at 150 model units, peaks at 176 model units and is at 173 after 4 hours, against a set point of 100. No insulin is made, so the feedback loop is broken and glucose stays high.
  • A small snack, type 2 diabetes. Glucose peaks at 120 model units and is at 108 after 4 hours, against a set point of 100. Insulin is made, but cells respond weakly to it, so glucose falls slowly.
  • A missed meal and a long walk, a typical body. Glucose dips to 90 model units, so glucagon rises and the liver releases glucose. It is back to 101 after 4 hours.
  • A missed meal and a long walk, type 1 diabetes, untreated. Glucose starts high at 150 model units and is still 141 after 4 hours, far above the set point of 100. With no insulin, the loop is broken and glucose stays high even without food.
  • A missed meal and a long walk, type 2 diabetes. Glucose dips to 90 model units, so glucagon rises and the liver releases glucose. It is back to 102 after 4 hours. This simple model leaves out diabetes medicines.

This is a simple qualitative model, not real patient data. Glucose is in model units with a set point of 100, not in mg/dL, and the hormone lines show relative amounts. The shaded band marks 90 to 110 model units. It shows the direction of each response, as described in the insulin and glucagon pages of You and Your Hormones, not real sizes or timings.

Diabetes is what happens when this loop fails. In type 1 diabetes, thought to be an autoimmune reaction, the body stops making insulin, and people need insulin every day. In type 2 diabetes, the body does not use insulin well; it develops over many years, and it makes up about 90 to 95% of diagnosed cases (see CDC). In type 2, there is too little insulin for the body's needs and the cells respond to it less, called insulin resistance (see You and Your Hormones). People who take insulin or some diabetes medicines can go dangerously low if they skip a meal and exercise, so they follow their care plan (see CDC and NIDDK).

Doctors use blood tests to diagnose diabetes. The CDC gives these ranges (see CDC):

TestNormalPrediabetesDiabetes
A1C testBelow 5.7%5.7 to 6.4%6.5% or above
Fasting blood sugar99 mg/dL or below100 to 125 mg/dL126 mg/dL or above
Glucose tolerance test, 2 hours140 mg/dL or below140 to 199 mg/dL200 mg/dL or above

From CDC. Only a doctor can diagnose diabetes.

5. Water balance

Keeping the right amount of water in the blood is called osmoregulation. Antidiuretic hormone, ADH, also called vasopressin, is made in the hypothalamus and released from the posterior pituitary gland (see You and Your Hormones).

When the blood gets too salty, osmoreceptors in the hypothalamus detect it and ADH is released. Low blood volume or pressure, sensed by baroreceptors, also triggers it. In the kidney, ADH makes the tubules take water back into the blood, so urine is more concentrated and less water is lost. Alcohol blocks ADH release, which is why it makes people pass more urine (see You and Your Hormones).

6. Endocrine glands

Endocrine glands have no ducts. They release hormones straight into the blood, which carries them around the body. Exocrine glands, like sweat glands, use ducts to carry their product to a surface (see SEER). The pancreas is both: one part sends digestive enzymes down a duct, and another part releases hormones (see SEER).

The pituitary is often called the master gland, because many of its hormones control other glands (see You and Your Hormones). A few of the main glands (see You and Your Hormones):

Explore: match the hormone to its gland

Turn on JavaScript to play. Here are the answers:

HormoneGland
Growth hormonePituitary SEER
MelatoninPineal SEER
ThyroxineThyroid SEER
Parathyroid hormoneParathyroids SEER
CortisolAdrenals SEER
Adrenaline, also called epinephrineAdrenals SEER
InsulinPancreas SEER
GlucagonPancreas SEER
OestrogenOvaries SEER
TestosteroneTestes SEER
Antidiuretic hormone, released into the bloodPituitary SEER

ADH is made in the hypothalamus but released from the pituitary (see You and Your Hormones).

7. How hormones act on cells

Hormones reach almost every cell, but only target cells with the matching receptor respond, like a key fitting a lock (see SEER). One hormone can cause different responses in different tissues. Adrenaline speeds up the heart, but makes the liver release sugar (see You and Your Hormones).

Protein and peptide hormones, like insulin, glucagon and oxytocin, cannot pass through the cell membrane. They bind receptors on the surface, which start a chain reaction inside the cell (see You and Your Hormones). The response is relatively rapid (see SEER).

Steroid hormones, like cortisol, oestrogen, progesterone and testosterone, are made from cholesterol and pass through the membrane. Their receptors are inside the cell, and some go into the nucleus and change how the cell uses its DNA (see You and Your Hormones). Because this works by making new proteins, it is relatively slow (see SEER).

8. Nerves and hormones compared

The two systems share the job of control, and they are linked: the brain controls the pituitary, and many hormones affect nerve cells (see You and Your Hormones).

Nervous systemEndocrine system
SignalElectrical impulses and neurotransmittersHormones in the blood
Speed and lengthSeconds, short-livedMinutes, hours or weeks
ReachLocal, to particular muscles or glandsMore general, to any cell with receptors

From SEER. The nervous system is covered in The Human Body.

9. How do we know?

The idea of a steady inside, and the chemicals that keep it steady, came together over about 60 years.

  1. 1865 Claude Bernard writes of the milieu intérieur, the internal environment that bathes the body's cells. (Libretti and Puckett)
  2. 1902 William Bayliss and Ernest Starling show that a chemical from the gut lining, secretin, triggers pancreatic juice even with the nerves cut. It is the first hormone discovered. (Bayliss and Starling; Dockray)
  3. 1905 Starling brings the word “hormone” into English. (Henderson; Starling)
  4. 1921 Frederick Banting and Charles Best, in J. J. R. Macleod's Toronto lab, make a pancreas extract that lowers blood sugar in diabetic dogs. J. B. Collip later purifies it for patients. (Rosenfeld)
  5. 1922 In January 1922, 14-year-old Leonard Thompson becomes the first patient treated with insulin. (Lambert and Delgado)
  6. 1923 Banting and Macleod share the Nobel Prize “for the discovery of insulin”. Banting gives half his prize money to Best. (Nobel Prize; Rosenfeld)
  7. 1926 Walter Cannon coins the word “homeostasis”. (Libretti and Puckett)
  8. 1929 Cannon sets out the idea in full in his review “Organization for physiological homeostasis”. (Cannon)

Quiz: Homeostasis check

Talk about it

  1. Why might positive feedback be dangerous if nothing stops it?
  2. Insulin and glucagon pull glucose in opposite directions. Why have two hormones instead of one?
  3. Our glucose model leaves out many things. Name two it ignores, and how they might change the curve.
  4. Why would the body use nerves for some jobs and hormones for others?

Sources

  1. Libretti, S. and Puckett, Y. (2023). Physiology, Homeostasis. StatPearls. Treasure Island, FL: StatPearls Publishing. PMID 32644564
  2. National Cancer Institute, SEER Training Modules. Characteristics of Hormones. cancer.gov
  3. National Cancer Institute, SEER Training Modules. Introduction to the Endocrine System. cancer.gov
  4. National Cancer Institute, SEER Training Modules. Endocrine Glands and Their Hormones. cancer.gov
  5. National Cancer Institute, SEER Training Modules. Pituitary and Pineal Glands. cancer.gov
  6. National Cancer Institute, SEER Training Modules. Thyroid and Parathyroid Glands. cancer.gov
  7. National Cancer Institute, SEER Training Modules. Adrenal Gland. cancer.gov
  8. National Cancer Institute, SEER Training Modules. Pancreas: Islets of Langerhans. cancer.gov
  9. National Cancer Institute, SEER Training Modules. Gonads. cancer.gov
  10. Society for Endocrinology, You and Your Hormones. Oxytocin. Last reviewed October 2023. yourhormones.info
  11. Zavyalova, E. G., Ustinov, N. B. and Kopylov, A. M. (2020). Exploring the efficiency of thrombin inhibitors with a quantitative model of the coagulation cascade. FEBS Letters 594: 995–1004. doi:10.1002/1873-3468.13684
  12. Osilla, E. V., Marsidi, J. L., Shumway, K. R. and Sharma, S. (2023). Physiology, Temperature Regulation. StatPearls. Treasure Island, FL: StatPearls Publishing. PMID 29939615
  13. Tansey, E. A. and Johnson, C. D. (2015). Recent advances in thermoregulation. Advances in Physiology Education 39: 139–148. doi:10.1152/advan.00126.2014
  14. Society for Endocrinology, You and Your Hormones. Insulin. Last reviewed May 2021. yourhormones.info
  15. Society for Endocrinology, You and Your Hormones. Glucagon. Last reviewed September 2021. yourhormones.info
  16. Centers for Disease Control and Prevention. Diabetes Basics. January 2, 2026. cdc.gov
  17. Centers for Disease Control and Prevention. Diabetes Testing. May 15, 2024. cdc.gov
  18. Society for Endocrinology, You and Your Hormones. Anti-diuretic hormone. Last reviewed October 2024. yourhormones.info
  19. Society for Endocrinology, You and Your Hormones. Glands. yourhormones.info
  20. Society for Endocrinology, You and Your Hormones. What is a hormone? Last reviewed August 2024. yourhormones.info
  21. Bayliss, W. M. and Starling, E. H. (1902). The mechanism of pancreatic secretion. The Journal of Physiology 28: 325–353. doi:10.1113/jphysiol.1902.sp000920
  22. Dockray, G. J. (2014). Gastrointestinal hormones and the dialogue between gut and brain. The Journal of Physiology 592: 2927–2941. doi:10.1113/jphysiol.2014.270850
  23. Henderson, J. (2005). Ernest Starling and ‘Hormones’: an historical commentary. Journal of Endocrinology 184: 5–10. doi:10.1677/joe.1.06000
  24. Starling, E. H. (1905). The Croonian Lectures: On the chemical correlation of the functions of the body. The Lancet 166: 339–341. doi:10.1016/S0140-6736(01)11877-5
  25. Lambert, C. and Delgado, E. (2024). 100 Years since the Discovery of Insulin, from Its Discovery to the Insulins of the Future. Biomedicines 12: 533. doi:10.3390/biomedicines12030533
  26. NIDDK (2021). Low Blood Glucose (Hypoglycemia). niddk.nih.gov
  27. CDC (2024). Low Blood Sugar (Hypoglycemia). cdc.gov
  28. Rosenfeld, L. (2002). Insulin: discovery and controversy. Clinical Chemistry 48: 2270–2288. PMID 12446492
  29. The Nobel Prize in Physiology or Medicine 1923. NobelPrize.org. nobelprize.org
  30. Cannon, W. B. (1929). Organization for physiological homeostasis. Physiological Reviews 9: 399–431. doi:10.1152/physrev.1929.9.3.399