Homeostasis and he Endocrine System
- In addition to the nervous system, mammals have a system of chemical coordination.
- Those chemicals which operate in a widespread way are called HORMONES, and are produced by ENDOCRINE GLANDS.
- These are transported in the blood to TARGET ORGANS in other parts of the body.
- The cells in these target organs have SPECIFIC RECEPTOR PROTEINS in the plasma membrane or in the cytoplasm.
Explain what makes a receptor protein specfic:
Each will have specific tertiary structure which only a hormone with a complementary shape will be able to bind to (Receptor has specific binding site).
Although different, both systems often interact and work together to coordinate body processes. E.g. in digestive juice secretion.
Nervous system and hormonal system comparison
- 1. Nervous system: Electrical communication by nerve impulses.
- 1. Hormonal system: Chemical communication by hormones.
- 2. Nervous system: Transmission is by neurones.
- 2. Hormonal system: Transmission by blood system.
- 3. Nervous system: Transmission is very rapid.
- 3. Hormonal system: Usuaully relatively slow.
- 4. Nervous system: Nerve impulses travel to specific parts of the body.
- 4. Hormonal system: Hormones travel to all parts of the body, only target cells respond.
- 5. Nervous system: Response is rapid.
- 5. Hormonal system: Response is slow.
- 6. Nervous system: Response is localised.
- 6. Hormonal system: Response is widespread.
- 7. Nervous system: Response is short-lived.
- 7. Hormonal system: Response is often long lasting.
- 8. Nervous system: Effect is temporary and reversible.
- 8. Hormonal system: Effect may be permanent and irreversible.
Homeostasis: The mechanism that maintains a constant internal environment (despite changes in the external environment).
Internal environment is the tissue fluid (filtered from blood) bathing all cells of the body.
Why is homeostasis important?:
- Biochemical reactions within the body are controlled by enzymes. Any changes in pH and temperature can alter the rate of these reactions amd, in extreme cases, enzymes and other proteins may denature.
- Water moves in and out of cells by osmosis. A constant water potential in tissue fluid prevents osmotic problems.
- The external environment in which many organisms live shows a wide range in abiotic factors, such as temperature. A constant internal environment allows a high degree of independence from these factors. This allows organisms such as mammals to live in areas ranging from the tropics to the arctic.
Features of the blood and tissue fluid which must be kept constant:
- Conc of glucose
- Water potential
- Conc of ions (e.g. Sodium, Potassium, Calcium)
The above factors are maintained within narrow limits due to negative feedback.
Negative feedback - a change from a SET POINT or level brings about mechanisms to return it to the set point, resulting in negative feedback loops.
Control of any self-regulating system involves a series of stages:
'Norm' or 'set point': deviation from the norm (Excess) -> detected by receptors -> Effectors stimulated and initiate corrective mechanisms -> restoration of the norm (negative feedback)
'Norm' or 'set point': deviation from the norm (Deficiency) -> detected by receptors -> effectors stimulated and initiate corrective mechanisms -> restoration of the norm (negative feedback)
A CONTROLLER is responsible for coordinating the information from receptors and sends it to effectors.
To a certain extent all animals exert some control over their internal temperature. This is important as if the temperature falls too low, biochemical reactions, controlled by enzymes, may become too slow for them to remain active. If it becomes too high, there is a risk of enzymes and other proteins denaturing.
ENDOTHERMS: Maintain a relatively constant body temperature largely indepenent of the environment. These are the animals that rely mainly on phsyiological mechanisms to control their internal temperature. Endotherms are also known as homeotherms.
Mammals and birds (Group of organisms that are endotherms)
ECOTHERMS: All other animals rely only on the external temperature and BEHAVIOURAL mecahisms to maintain a reasonaly constant internal environment. E.g. a lizard will move between the sun and the shade.
TEMPERATURE REGULATION IN ENDOTHERMS.
Although endotherms maintain a stable CORE body temperature, the temperature of their EXTREMITIES may be cooler than this.
Most mammals have core body temps ranging from 35 - 40 degrees. Humans maintain their core body temp at 37 degrees. In birds this is 40 - 44 degrees.
Heat can be transferred by conduction, convection and radiation.
- Conduction: transfer of heat energy between molecules
- Convection: transfer of heat due to movement of molecules (in fluids)
- Radiation: heat transfer due to emission of electromagnetic waves of the body
temp regulation in endotherms continued..
Changes in the external temperature are detected by temperature receptors in the skin. These send nerve impulses to the brain, which initiates appropriate responses (behavioural and physiological).
Examples of behavioural responses include:
- Changing position, e.g. curling up to reduce surface area and reduce heat loss by convection and radiation
- Putting on or taking off clothes
- Turning heat up or down/consuming hot or cold drinks
- Increasing or decreasing movement
THE HYPOTHALAMUS is the CONTROLLER and it contains a THERMOREGULATORY CENTRE. This is further subdivided into:
- THE HEAT GAIN CENTRE which operates when blood temperature decreases and brings about mechiansms to GENERATE heat and CONSERVE existing heat.
- THE HEAT LOSS CENTRE which operates when blood temperature increases and brings about mechanisms causing heat to be LOST.
The temperature receptors in the skin send nerve impulses to the hypothalamus in the brain. Within the hypothamaus itself, there are also temperature receptors that monitor the temperature of the blood flowing through it (i.e. the internal temp). The hypothalamus acts via the autonomic (involuntary) nervous system, to initiate appropriate physiological responses.
a) heat conservation mechanisms
- Nerve impulses along SYMPATHETIC nerves from the hypothalamus cause muscles in the walls of the SKIN ARTERIOLES to CONTRACT.
- This causes the lumen of the arterioles to CONSTRICT.
- In addition, SHUNT VESSELS DILATE, diverting blood away from the skin's capillaries.
- Both result in LESS blood flow to the skin surface and LESS heat loss by RADIATION.
- This is known as PILOERECTION.
- Nerve impulses from the hypothalamus cause erector pili muscles at the base of the hairs in the skin to CONTRACT.
- This causes hairs on the skin to become erect.
- In hairy mammals, raising the hair makes the fur 'thicker' trapping more air, proving extra insulation.
- In humans this mechanism is not very effective and only results in goose bumps.
- Form of heat transfer this effects: mainly convection.
b) Heat gain mechanisms
INCREASED METABOLIC RATE
- The hypothalamus sends nerve impulses to the adrenal gland, causing the secretion of the hormone ADRENALINE.
- This increases the rate of metabolism, increasing heat production.
- Exposure to cold conditions for long periods of time causes stimulation of the thyroid gland and the secretion of THYROXINE (another hormone), which also results in an increase in metabolic rate.
- Involves rapid, involuntary contractions of skeletal muscle.
- Gains heat for the body by: respiration rate increases in muscle cells to provide energy for contraction and the heat energy is released from respiration.
- Some mammals have layers of a special tissue called brown fat situated just under the skin. Impulses from the hypothalamus cause the cells in this tissue to rapidly oxidise fatty acids to release energy as heat.
All of the aboe mechanisms are controlled by the heat gain centre.
c) Mechanisms controlled by the heat loss centre
- Nerve impulses along SYMPATHETIC nerves from the hypothalamus cause muscles in the walls of the skin arterioles to RELAX.
- This causes the arterioles to DILATE.
- More blood flows tto the skin surface and more heat is lost by RADIATION.
In hot conditions:
- Skin arterioles are dilated
- Sphincter muscles are relaxed
- Shunt vessels are constricted
- Blood flow to the skin capillaries is increased
In cold conditions:
- Skin arterioles are constricuted
- Sphincter muscles are contracted
- Shunt vessels are dilated
- Blood flow to the skin capillaries is decreased
DECREASED METABOLIC RATE
- Less adrenaline and thyroxine are secreted, decreasing metabolic rate, hence decreasing heat production.
- Vasodilation increases blood flow to the sweat glands resulting in more sweat being secreted onto the surface of the skin.
- The water in the sweat EVAPORATES using heat energy from the body, leading to a cooling effect.
- Humans have sweat glands over the whole body, making this mechanism very efficient.
- Animals with fur have sweat glands confined to areas where fur is absent, e.g. pads of the feet. The efficiency of sweating is affected by the humidity.
- Activity of brown fat cells is reduced
PHSYIOLOGICAL reponse to COLD:
Stimulus: decrease in temp
Receptors: temp receptors in skin and hypothalamus
Co-ordinator: hypothalamus (heat gain centre)
Effectors: skeletal muscles, muscles in skin arteriole walls, hair erector pili muscles, adrenal and thyroid glands
Responses: shivering, vasoconstriction, piloerection, increased metabolic rate
INCREASE in blood temp/impulses from skin warm receptors -> detected by thermoreceptors in the heat loss centre of the hypothalamus -> impulses via motor neurons -> vasodilation:increased blood flow to capillaries; increased sweating; skin hairs lowered by relaxation of erector muscles; decrease in metabolic rate -> restoration of the norm (negative feedback)
DECREASE in blood temp/impulses from skin cold receptors -> detected by thermoreceptors in the heat gain centre of the hypothalamus -> impulses via motor neurons -> vasoconstriction:reduced blood flow to capillarie; sweating inhibited;piloerection-hairs raised by contraction of erector muscles; inncreased muscular activitity-shivering; increase in metabolic rate -> restoration of the norm (negative feedback)
Positive feedback and temperature control
POSITIVE FEEDBACK occurs when the responses to the change cause further deviation from the set point. (e.g. oestrus cycle), but it often arises when there is a breakdown of a control system.
- Is an elevated body temp due to failed thermoregulation
- It can be caused by prolonged exposure to excessive heat
- The heat regulating mechanisms of the body (eg sweating) eventually become overwhelmed and unable to effectively deal with the heat, causing the body temp to climb uncontrollably
- The high temp causes enzymes to work faster, increasing metabolic rate, which in turn produces more heat, causing enzymes to work even faster etc.
- Enzymes may eventually denature
- Hyperthermia differs from fever in that the elevated body temp in fever is caused by a change in the hypothalamus set point, e.g. due to infection.
- Uncontrolled positive feedback is possible but usually prevented by theromoregulation, which first acts to raise the body temp to, but then maintains it at, the new set point (until the fever 'breaks')
- If the body gets too cold, the temperature regulating system also breaks down, and positive feedback results in a cold person becoming even colder.
- This time this is as enzymes slow, metabolic rate falls so less heat is produced.
- Enzymes fall further below their optimum, slow down reactions more so a downward spiral eventually may lead to death.
Temperature regulation in ectotherms
Animals like desert reptiles rely mainly on BEHAVIOURAL mechanisms to control their body temperature.
BEHAVIOUR CONTROL MECHANISMS include:
- Basking in the sun in the early morning to gain the initial heat needed to become active
- Shifting between sun and shade as temperatures rise towards midway
- Changing posture to vary the surface area exposed to direct sunlight
- Retreating to their burrow during the hottest part of the day to stay cool (or during the night to stay warm)
- Emerging in the evening and hunting for food
Some PHYSIOLOGICAL MECHANISMS can also occur in certain lizards:
- Contraction of black pigment cells to make the skin lighter during warmer times (absorns less heat if paler - assists in the control of body temp)
- Redirecting blood flow to different regions at different times of day (less blood at body surface, e.g. to lose less heat if envrionment is too cold - assists in the control of body temp)
The Control of Blood Glucose Concentration
In humans blood glucose levels are maintained at around 90mg per 100cm3 (5-5.6 mmol/l). It is important to regulate blood glucose as:
- It is the main respiratory substrate. The blood is the brains only source of glucose.
- Changes in blood glucose concentration can alter water potential of blood and tissue fluid.
Some organs, such as the brain, are unable to store carbohydrate and so cannot function without a constant supply of glucose from the blood. There are many factors which influence blood glucose concentration. These include:
- Dietary intake and digestion of carbohydrates (and absorption of glucose)
- GLYCOGENESIS (formation of glycogen) - the conversion of glucose to glycogen, which can be stored.
- GLYCOGENOLYSIS - the breakdown of stored glycogen into glucose.
- GLUCONEOGENESIS - (formation of glucose from other sources) - conversion of non-carbohydrate sources, such as amino acids, into glucose.
- Rates of respiration
The role of the pancreas (produces enzymes)
The pancreas contains groups of cells called the Islets of Langerhans which contain receptors that are sensitive to blood glucose levels. There are 2 types of islet cells:
- ALPHA CELLS - which produce the hormone GLUCAGON in response to LOW blood glucose levels
- BETA CELLS - which produce the hormone INSULIN in response to HIGH blood glucose levels
(Insulin makes it easier for glucose to get into cells)
Glycogen - made up of lots of alpha glucose and is stored in the liver and is also branched so lots of glucose can attach
Insulin and glucagon = proteins
^ glucagon promotes this.
Liver produces glucose.
Responses to HIGH blood glucose conc.
- After a meal high in carbohydrates, blood glucose levels will be above normal.
- This is detected by the RECEPTORS in the Islets of Langerhans, causing the BETA cells to produce INSULIN.
- This is released into the BLOOD and travels to its TARGET CELLS.
- These are mainly the LIVER and muscle cells but also involve other cells.
- INSULIN then binds to SPECIFIC GLYCOPROTEIN RECEPTORS on the target cell membrane.
This causes a reduction in blood glucose levels by:
- INCREASING THE UPTAKE OF GLUCOSE BY THE CELLS. Glucose usually enters cells by facilitated diffusion through specific carrier protein molecules. Extra carrier molecules are present in the cells cytoplasm. Insulin causes these to be inserted into the cell membrane so the permeability increases.
- Insulin ACTIVATES ENZYMES which convert glucose to glycogen (in liver and muscle cells) which can then be stored. This is known as GLYCOGENESIS.
- Insulin ACTIVATES ENZYMES which convert glucose to fats for storage in adipose tissue.
- INCREASING RESPIRATION RATES in cells.
Responses to LOW blood glucose concentration
- When the Islets of Langerhans detect a FALL in blood glucose levels the ALPHA CELLS produce the hormone GLUCAGON
- This hormones main target cells are the liver cells
- GLUCAGON binds to specific protein receptors on the target cell membrane.
This causes an INCREASE in blood glucose levels by:
- Activating enzymes which catalyse the conversion of glycogen to glucose. This is known as GLYCOGENOLYSIS.
- Glucagon also stimulates the conversion of amino acids and glycerol to glucose. This is known as GLUCONEOGENESIS.
ADRENALINE also RAISES blood glucose levels in 2 ways:
- Activating an enzyme that causes breakdown of glycogen to glucose
- Inactivating an enzyme that synthesises glycogen from glucose
The glucose then passes out of the cells and into the blood, RAISING blood glucose levels.
The second messenger model of hormone action
The hormones involved in glucose homeostasis exert some of their effects in cells by stimulating production of another chemical known as a SECOND MESSENGER. (Look at pg 11 for diagram)
- The hormone adrenaline/insulin/glucagon approaches receptor site. (adrenaline/insulin/glucagon = 1st messenger)
- Adrenaline fuses to receptor site, and in doing so activates an enzyme inside the membrane.
- The activated enzyme converts ATP to cyclic AMP, which acts as a SECOND messenger that activates other enzymes that, in turn, convert glycogen to glucose.
SECOND messenger needed so hormones can get into cells.
KEY FEATURES OF THE MODEL ARE:
- The hormone (first messenger) binds to specific RECEPTORS on the target cell membranes, forming a hormone-receptor complex.
- This complex activates an enzyme that results in the production of a chemical known as a second messenger (e.g. cAMP) in the cell.
- This second messenger causes a series of chemical changes leading to the response. For glucagon and adrenaline, the response is the conversion of glycogen to glucose. Insulin uses a similar second messenger system to cause glucose to be converted to glycogen.
control of blood glucose is e.g. of negative feedb
Normal blood glucose level..
RISE in blood glucose -> detected by the BETA cells of the Islets of Langerhans in the pancreas -> INSULIN SECRETION -> activation of enzymes that promote the conversion of glucose into glycogen in liver and muscle tissue. increase in the permeability of body cells to glucose (by promoting the synthesis of more membrane proteins). activation of enzymes that promote fat synthesis. -> restoration of the norm (negative feedback)
FALL in blood glucose -> detected by the ALPHA cells of the Islets of Langerhans in the pancreas -> GLUCAGON SECRETION -> activation of enzymes that promote the conversion of glycogen into glucose in liver tissue and fatty acid release in adipose tissue. activation of enzymes that promote the conversion of non-carbohydrates, such as amino acids, into glucose (gluconeogensis)
DIABETES MELLITUS - This is a disease where the body is no longer able to control blood glucose levels effectively. There are 2 types of diabetes mellitus:
TYPE 1 - Also known as INSULIN DEPENDENT or JUVENILE ONSET
- CAUSE - Inability to produce insulin. It usually appears in childhood. The body's own immune system may destroy the Beta cells. This is known as autoimmune response.
- TREATMENT - Blood glucose levels must be monitored regularly. This can be done using a glucose BIOSENSOR. Insulin can be given by INJECTION, but the amount must match glucose intake. Diabetics must also manage their diets and levels of exercise. Care must be taken to balance diet and insulin to avoid hypoglycaemia (where glucose levels drop too low).
- Glucose cannot be given orally because it would be digested by enzymes (as it's a protein/hormone)/denatured by stomach acid and is also too large to be absorbed.
Diabetes mellitus continued
TYPE II - also known as INSULIN INDEPENDENT or LATE ONSET
CAUSE - Gradual loss in the responsiveness of target cells to insulin, due to receptor abnormalities. This type is more common and usually occurs later in life.
TREATMENT - Can be managed by careful regulation of diet, especially sugar intake and balancing this with the amount of exercise taken.
- High levels of blood glucose means that the kidney is unable to reabsorb all the glucose filtered back into the blood. This results in the presence of large amounts of glucose in the urine.
- Persistent thirst.
- Frequent urination.
- Craving for sweet foods.
Diagnostic test - the glucose tolerance test
Involves the patient swallowing a glucose solution after a period of at least 8 hours of fasting. A base blood glucose level is taken before a standard glucose load is taken in. The blood glucose levels are then checked at regular intervals for 2-3 hours.
The mammalian Oestrus cycle
4 major hormones involved in the Oestrus cycle:
- FSH (Follicle Stimulating Hormone) - secreted into the blood from the anterior lobe of the pituitary gland
- LH (Luteinising hormone) - secreted into the blood from the anterior lobe of the pituitary gland
- Oestrogen - secreted by the developing follicles in the ovary
- Progestrone - secreted by the corpus luteum of the ovary
The female reproductive system and the oestrus cycle
- From the onset of puberty the human female reproductive system undergoes cyclic changes knwo as the oestrus cycle. This cycle actually occurs in all female mammals with varying frequency. In humans it occurs once every month and is also known as the menstrual cycle. (look @ pg 14 for diagram)
- Stages in the human oestrus cycle
- Human females are born with almost a million follicles in the 2 ovaries
- Approx. 500 of these will develop into mature Graafian follicles, which release mature eggs (or ova)
- Every 28 days or so 1 mature ovum will be released by an ovary. This process begins at the onset of puberty (at around 12 yrs old) and continues every month for about 40 years.
- Day 1 is taken as the onset of menstruation, when the endometrium (uterus lining) is shed. The cycle is controlled by hormones and is a good example of how feedback loops operate
- FSH is released into the blood from the pituitary gland
- FSH travels to the ovary where it stimulates one of the follicles to develop into a GRAAFIAN FOLLICLE, which consists of an oocyte (immature ovum) surrounded by follicle cells
- Follicle cells produce low levels of OESTROGEN as they develop
- LOW oestrogen levels INHIBIT FHS production by NEGATIVE FEEDBACK
- As the follicle continues to grow, HIGHER levels of oestrogen are released and this stimulates the pituitary gland to release LH
- The RISE in LH (and FSH) causes OVULATION - the ovum is released
- The ruptured Graafian follicle becomes a structure called the CORPUS LUTEUM
- The corpus luteum produces PROGESTRONE, which inhibits FSH and LH production
- If fertilisation does not occur, the corpus luteum degenerates so progestrone production decreases, triggering menstruation (shedding of the endometrium)
- FSH production is no longer inhibited so more FSH is released and the cycle starts again
Look at pg 15 for graphs
What hormonal changes indicate ovulation: Surge in LH. & Start of rise in progestrone
Summary of hormone action
- Hormone: Follicle stimulating hormone/FSH
- Site of secretion: Pituitary gland
- Target cells: Follicle cells in ovary
- Function: Stimulates development of follicle AND production of oestrogen by follicle cells
- Hormone: Oestrogen
- Site of secretion: Follicle cells of ovary
- Target cells: Anterior pituitary and endometrium of uterus
- Function: Normal levels inhibit FSH production AND High levels stimulate FSH and LH production AND repairs endometrium
- Hormone: Luteinising hormone/LH
- Site of secretion: Pituitary gland
- Target cells: Ovaries
- Functions: Ovulation AND development of corpus luteum which produces progestrone
- Hormone: Progestrone
- Site of secretion: Corpus luteum of ovary
- Target cells: Pituitary gland and endometrium
- Function: Inhibits FSH and LH production AND thickens & maintains endometrium in prep for implanation of fertilised egg
- The oestrus cycle in other mammals is similar to that in humans
- Adaptations usually involve the timing of the events of reproduction
- Often in wild animals the onset of the oestrus cycle is stimulated by changes in day length or temperature
- A region of the brain called the hypothalamus released another hormone, GnRH in response to these changes
- This hormone stimulates the release of FSH and starts the cycle
Change in day length is likely to be more reliable stimulus than temp changes because it changes in a predictable way/constant way
The behaviour and physiology of many female mammals changes around ovulation. These changes are correctly known as OESTRUS but are also referred to using different terms such as: in season/on heat
The female fox is only receptive to males for about 3 weeks in late January. Her gestation time is 7-8 weeks. Relate these facts to the survival chances of her young: Young born in Spring. Maximum chances of survival as more resources available.
Co-ordination at a cellular level is achieved by chemical mediators, released by some mammalian cells to act locally on the cells producing them and other cells in their immediate vicinity.
PROSTAGLANDINS and HISTAMINE are examples of chemical mediators. They are secreted by infected or damaged cells to produce the inflammatory response to injury.
There are a few differences between chemical mediators and hormones:
- Chemical mediators can be secreted from cells all over the body (not just glands)
- Their target cells are right next to where the mediators are produced, thus stimulating a LOCAL response (not a widespread one)
- They only have to travel a short distance to their target cells, by diffusion, so produce a quicker response than hormones (transported in the blood)
PROSTAGLANDINS are released from damaged cells at the site of an injury and cause:
- VASODILATION of ARTERIOLES to increase blood flow and bring more phagocytic white blood cells to the area
- Clotthing of the blood to minimise blood loss and entry of pathogens
- They also stimulate histamine production
HISTAMINE is released by MAST CELLS (a type of white blood cell found in connective tissue). It acts on CAPILLARY walls, causing them to become MORE PERMEABLE. Plasma (containing proteins) and phagocytes leave the blood and enter the damaged tissues. Histamine is also released in response to allergens, causing an allergic reaction.
Typical characteristics of INFLAMMATION include redness, heat, swelling and pain. For each of these effects explain what causes it and the advantages: