CB7 · Animal coordination, control and homeostasisTopic 7 — Animal coordination, control and homeostasis
Hormones, reproduction and blood-glucose control.
Revise the key ideas
Hormones and endocrine glands
The nervous system sends rapid electrical signals along neurones. Hormonal communication uses chemical messengers carried in the blood and is usually slower, with longer-lasting effects.
Endocrine glands release hormones directly into the bloodstream. Blood carries a hormone around the body, but only target cells with suitable receptors respond to it.
A target organ is an organ affected by a particular hormone. A hormone may affect several target tissues; it does not act on every cell it passes.
The pituitary gland lies at the base of the brain. It releases FSH, LH and growth hormone, and hormones such as TSH that influence other endocrine glands.
The thyroid gland in the neck produces thyroxine. The adrenal glands above the kidneys produce adrenalin; adrenaline is an alternative spelling.
The pancreas produces insulin and glucagon. The ovaries produce oestrogen and progesterone; the testes produce testosterone.A hormone directory: target cells respond through suitable receptors.
Growth hormone supports growth of bones and other tissues. Puberty involves changes in sex hormones and growth-hormone activity; it is an oversimplification to say that sex hormones alone directly make the pituitary release growth hormone.
Homeostasis and negative feedback
Homeostasis maintains a stable internal environment despite changes inside or outside the body. Examples include blood glucose concentration, body temperature and water balance.
Stable does not mean perfectly unchanging: conditions fluctuate around suitable levels. Maintaining these levels helps cells and enzymes function effectively.
Negative feedback reverses a change from the normal level. If a level rises too high, the response brings it down; if it falls too low, the response brings it up. The response gets smaller as the level returns towards normal.
If a regulated level rises too far, feedback can reduce it; if it falls too far, feedback can raise it. The response must oppose the change, rather than amplify it.
Negative feedback is a control mechanism, while homeostasis is the maintenance of the internal environment. The two terms are related but are not identical definitions.
Thyroxine and its feedback pathway
Thyroxine helps control metabolic rate: the rate at which chemical reactions occur in the body. It also supports growth and development.
When blood thyroxine concentration is low, the hypothalamus releases more TRH, thyrotropin-releasing hormone.
TRH stimulates the pituitary gland to release TSH, thyroid-stimulating hormone.
TSH stimulates the thyroid gland to produce and release thyroxine into the blood.
When thyroxine returns to a suitable level, it reduces (inhibits) further TRH release and TSH production. The thyroid receives less stimulation, so it does not keep producing too much thyroxine.
This is negative feedback: the increase in thyroxine reduces the signals that caused its production. Do not confuse the thyroid, which makes thyroxine, with the pituitary, which makes TSH.Thyroxine inhibits its stimulating signals: an example of negative feedback.
Adrenalin: fight or flight
Adrenalin is released from the adrenal glands during frightening or exciting situations. It prepares the body for a rapid fight-or-flight response.
It increases heart rate and blood pressure, and increases blood flow to skeletal muscles. This helps deliver more oxygen and glucose for respiration.
Adrenalin stimulates the liver to break glycogen down into glucose and release glucose into the blood. Glycogen is a stored carbohydrate; glucose is the circulating sugar.
Adrenalin changes where blood flows: vessels supplying skeletal muscles widen (dilate), while vessels in some other regions narrow. More blood reaches the muscles to support rapid activity.
The nervous system and hormones can work together. An adrenalin response is a temporary preparation for activity, rather than the same long-term control pathway as thyroxine.
The menstrual cycle and fertilisation
The menstrual cycle prepares the uterus for a possible pregnancy. An egg matures and is released. Cycles start during puberty and stop at menopause; their length and the ages at which they start and stop vary.
Day 1 is the first day of menstruation. The uterus lining is shed when hormone levels fall; menstruation is not simply the loss of an egg.
After menstruation, the lining is repaired and thickens under the influence of oestrogen. It does not wait until a fixed day 11 to begin repairing.
Ovulation is the release of an egg from an ovary. In a simplified 28-day cycle it occurs around day 14, but actual timing varies with the cycle.
After ovulation, progesterone helps maintain the thickened uterus lining. If pregnancy does not occur, progesterone and oestrogen fall and another menstruation begins.
Sperm can travel through the cervix and uterus to an oviduct. Fertilisation is the fusion of sperm and egg nuclei, usually in an oviduct, also called a fallopian tube.
The fertilised egg divides to form an embryo as it moves towards the uterus. Implantation is the embryo attaching to the uterus lining; it is different from fertilisation.
Fertilisation is associated with the time around ovulation, not a fixed day 17–21 window. A textbook 28-day example cannot reliably predict an individual's fertile days.
Interactions of FSH, LH, oestrogen and progesterone
FSH, follicle-stimulating hormone, is released by the pituitary. It stimulates an ovarian follicle containing an egg to mature and encourages oestrogen production.
The developing follicle produces oestrogen. Oestrogen repairs and thickens the uterus lining and inhibits FSH for much of the cycle.
A high oestrogen level just before ovulation stimulates an LH surge. This is a change in its feedback effect; do not assume oestrogen always inhibits every pituitary hormone.
The pituitary releases LH (luteinising hormone). A sharp rise in LH triggers ovulation. The emptied follicle then forms a structure called the corpus luteum.
After ovulation, the corpus luteum produces progesterone. This maintains the uterus lining and reduces (inhibits) FSH and LH release, helping prevent another follicle maturing and another egg being released in the same cycle.
If pregnancy does not occur, the corpus luteum breaks down and progesterone and oestrogen decrease. The lining is shed and reduced inhibition allows FSH to rise for the next cycle.Sequence if pregnancy does not occur; actual cycle lengths and timings vary.
When interpreting a hormone graph, look for an oestrogen rise before ovulation, a sharp LH surge around ovulation and a progesterone rise afterwards. These are schematic patterns, not identical curves in every person.
Hormonal and barrier contraception
Contraception reduces the chance of pregnancy. Different methods act in different ways, so preventing ovulation and blocking sperm should not be described as the same mechanism.
The combined contraceptive pill contains oestrogen and a progestogen, which acts like progesterone. These hormones suppress pituitary FSH and LH and prevent ovulation.
Progestogen can also thicken cervical mucus, making it harder for sperm to pass. Hormonal methods can include pills, patches, injections and implants; their mechanisms and suitability vary.
A condom is a barrier that prevents semen and sperm entering the vagina when used correctly. Condoms also reduce transmission of many sexually transmitted infections; hormonal contraception does not provide that protection.
A diaphragm covers the cervix and is used with spermicide to reduce sperm entry into the uterus. It does not stop the ovaries releasing eggs.
Evaluate a method using effectiveness, correct use, possible side effects, how long it lasts, reversibility and protection against infections. No method should be described as guaranteed to prevent every pregnancy.
A daily pill requires consistent use; a long-acting method reduces that daily requirement but can need a healthcare procedure. Barrier methods avoid altering the menstrual hormones but also depend on correct use.
Assisted reproductive technology
Assisted reproductive technology, or ART, can help some people with fertility problems. The approach depends on the cause of the difficulty and does not guarantee a pregnancy.
Clomifene is a fertility medicine that can encourage ovulation in people who do not ovulate regularly. It promotes pituitary release of FSH and LH by reducing the effect of oestrogen feedback.
In IVF, in vitro fertilisation, fertility hormones such as FSH stimulate development of several follicles. A hormone trigger, often acting like LH, helps eggs complete maturation before collection.
Eggs are collected and fertilised with sperm in a laboratory. Embryos are allowed to develop before a selected embryo is transferred into the uterus.
Progesterone can be given to help support the uterus lining after embryo transfer. Laboratory fertilisation and transfer do not guarantee implantation or a live birth.IVF involves laboratory fertilisation followed by embryo transfer.
Benefits include the possibility of pregnancy despite some fertility problems. Limitations include cost, physical and emotional demands, variable success and risks such as excessive ovarian stimulation or multiple pregnancy.
Evaluate success using comparable data and the stated outcome, such as pregnancy or live birth. Age and the cause of infertility can affect success, so results from different groups are not automatically comparable.
Insulin, glucagon and blood glucose
Blood glucose concentration rises after absorption of carbohydrate from food and can fall as cells use glucose. The pancreas monitors and responds to these changes.
When blood glucose is high, the pancreas releases more insulin. Insulin promotes glucose uptake by body cells and promotes conversion of glucose into glycogen in the liver and muscles.
As blood glucose returns towards a suitable level, insulin secretion decreases. This is a negative-feedback response to an increase in glucose.
When blood glucose is low, the pancreas releases more glucagon. Glucagon stimulates the liver to break glycogen down into glucose and release it into the bloodstream.
As blood glucose rises towards a suitable level, glucagon secretion decreases. Insulin and glucagon therefore have opposing effects on blood glucose.Insulin and glucagon have opposing effects; secretion decreases as glucose returns towards normal.
Glucose and glycogen are not interchangeable names: glucose is a small sugar that circulates in blood, while glycogen is a storage carbohydrate made from glucose units.
Glucagon and glycogen are also different: glucagon is a hormone, while glycogen is a stored carbohydrate. The liver can supply glucose to the blood between meals.
Type 1 and type 2 diabetes
In type 1 diabetes, the body's immune system destroys insulin-producing pancreatic cells, so little or no insulin is produced. Blood glucose can become too high.
Type 1 diabetes is controlled with insulin delivered by injections or a pump, together with blood-glucose monitoring and appropriate management of food and activity. Diet alone cannot replace the missing insulin.
In type 2 diabetes, cells respond less effectively to insulin, and the pancreas may also produce insufficient insulin. This is often described as insulin resistance.
Type 2 diabetes may be managed with dietary changes, physical activity and medicines; some people also need insulin. It should not be described as always controlled by diet and exercise alone.
A higher body mass and greater abdominal fat are associated with increased type 2 diabetes risk, but genetics, age and other factors also matter. Type 2 diabetes can occur without obesity.
Glucose may appear in urine if blood glucose becomes high enough. This can be a sign of diabetes, but a urine result alone cannot confirm a diagnosis.
BMI, waist:hip ratio and interpreting risk
Body mass index, BMI, is calculated as mass in kilograms divided by height in metres squared: BMI = mass (kg) ÷ [height (m)]².
For a mass of 81 kg and height of 1.80 m, BMI = 81 ÷ 1.80² = 25. Square the height before dividing, and convert centimetres to metres first.
Common adult categories are below 18.5: underweight; 18.5 to below 25: healthy-weight range; 25 to below 30: overweight; 30 or above: obesity. These adult boundaries are not used directly to assess children and teenagers, whose age and sex are considered.
Waist:hip ratio = waist circumference ÷ hip circumference. Use the same units for both measurements; the ratio has no unit.
For a waist of 80 cm and hips of 100 cm, the ratio is 0.80. A greater proportion of abdominal fat is associated with increased type 2 diabetes risk.
A positive correlation means that higher values of one variable tend to occur with higher values of another. A trend between BMI and diabetes risk is not proof that every person with a high BMI will develop diabetes.
BMI does not distinguish muscle from fat or show where fat is stored. Waist:hip ratio provides different information, but neither measure alone describes an individual's complete health or proves causation.
Using data and practical evidence
Compare diabetes risk using proportions or percentages when group sizes differ. Ten cases out of 100 people and ten cases out of 1,000 people are different rates despite the same case count.
Percentage = number in a group ÷ total number × 100. For example, 12 cases in 200 people is 6%; state which population the percentage describes.
Check whether differences in age, activity or other factors could affect a reported correlation. A large sample and comparable groups support a more reliable comparison.
Benedict's test can investigate reducing sugars in simulated urine: add Benedict's reagent and warm in a hot-water bath under school instructions. A colour change from blue towards green, yellow, orange or brick-red indicates reducing sugar.
Benedict's reagent detects reducing sugars, not only glucose. Use simulated samples, appropriate eye protection and controlled heating; compare with a known positive and a negative control.
A colour test on a simulated sample illustrates the chemistry of sugar detection. It does not diagnose diabetes or replace blood-glucose monitoring.
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