9 - Internal Regulation Flashcards
Homeostasis
Vast amount of energy used towards maintaining a set point (range).
Set point: a single value that the body works to maintain eg levels of water, oxygen, glucose, calcium, protein, fat, and acidity in the body.
Allostasis
The adaptive way in which the body anticipates needs depending on the situation.
Constantly reacting to changes, anticipates changes eg more body fat for winter.
Allostatic load: cost associated with performing homeostatic adjustments
Poikilothermic (ectothermic)
Body temperature matches that of the environment.
The organising lacks the internal, physiological mechanisms of temperature regulation.
Instead, external sources and behavioural adaptation are used to regulate temperature eg moving into the sun, huddling together.
Homeothermic (endothermic)
Internal physiological mechanisms used to maintain body temperature.
Also may utilise behavioural adaptations.
Requires high rates of energy.
E.g. sweating, panting, vasoconstriction/vasodilation
Why control body temperature?
Mammals evolved to have a constant temperature of 37 degrees c.
Pros: muscle activity benefits from being as warms as possible.
Cons: maintaining a higher body temp increases energy demand.
Proteins (amino acid chains) are damaged at higher temps.
Brain mechanisms of temperature regulation
Temperature regulation is largely dependent upon areas of the hypothalamus:
Preoptic area (POA): physiological responses
Anterior hypothalamus (AH): behavioural responses
POA/AH receives input from temperature receptors in the skin, and brain and other organs. Also receives input from the immune system.
POA/AH controls shivering, sweating, heart rate, blood flow to skin etc. So if too hot, tells body to sweat etc.
Mechanisms of water regulation
Mechanisms of water regulation are vital for survival.
We have evolved to maintain a consistent concentration of salt in body fluids (approx 0.9%)
Achieved by monitoring the balance of extra cellular and intercellular fluids.
Water moves across the cell membrane via aquaporins
Angiotensin II
The angiotensin cascade:
Angiotensinogen is a hormone circulating the blood.
An enzyme released by the kidneys (renin) converts angiotensinogen to angiotensin I.
An enzyme converts angiotensin I to angiotensin II.
Angiotensin II acts to constrict blood vessels and increase blood pressure via circumventricular organs.
Vasopressin
Is an antidiuretic hormone released by the posterior pituitary.
Raises blood pressure by constricting blood vessels.
Helps to compensate for decreases water volume.
Enables the kidneys to reabsorb water and excrete highly concentrated urine.
Angiotensin II influences the release of vasopressin from the pituitary.
Thirst
Osmotic thirst
Hypovolemic thirst
Osmotic thirst
Concentration of solutes inside and outside a cell create osmotic pressure.
Water flows across a semi-permeable membrane from an area of low solute concentration to an area of high solute concentration.
Osmotic pressure occurs when solutes are more concentrated on one side of the membrane.
Triggers osmotic thirst: a drive for water that helps restore the normal state.
Hypovolemic thirst
Thirst associated with low volume of body fluids.
Overall loss in extra cellular fluid volume through vomiting, blood loss, diarrhoea etc.
Not necessarily a change in solute concentration.
Causes a drop in blood pressure that is detected by baroreceptors:
Initiates mechanisms of decreasing the production of urine (vasopressin) and the construction of blood vessels (angiotensin II).
Initiates sodium-specific thirst (need more water + solutes eg Gatorade)
Food and energy regulation
Regulation of eating/energy stores is vital for survival.
System for controlling food intake is far more complex than those used in in temp regulation and thirst.
Food intake is important for energy and nutrient supply (essential amino acids are found in our diet)
Energy and nutrient reserve must be maintained.
Short-term regulation of feeding
Oral factors:
The desire to taste and chew are motivating factors in hunger and satiety eg chewing gum
Sham feeding experiments show that tasting and chewing food is not enough to give us the sensation of being full.
The stomach and intestines
The main signal to stop eating is the distension of the stomach
The vagus nerve
Conveys information about the stretching of the stomach walls to the brain
Splanchnic nerves
Convey information about the nutrient contents of the stomach
Duodenum
Part of the small intestine
Site of initial nutrient absorption
Distention of the duodenum can also produce feelings of satiety.
The duodenum also released the hormone cholecystokinin (CCK), which helps to regulate hunger.
Significant increases in CCK release in sufferers of anorexia
Glucose
Carbohydrates in our diet are broken down into sugars.
Glucose is the principle sugar used by the body for energy.
Particularly important source of energy for the brain.
Insulin
Hormone released by the pancreas that enables glucose to enter the cell via glucose transporters.
Sensory stimuli l, digestive tract, and liver signal the release of insulin from the pancreas.
Insulin acts to convert unused glucose into glycogen, which is stored mainly in the liver and muscles (glycogenesis)
Glucagon
Hormone released by the pancreas when glucose levels fall.
Stimulates the liver to concert some of its stored glycogen to glucose.
Triggered by low concentrations of glucose in the blood.
Long-Term Regulation of Feeding
Long-term regulation of food intake involves the monitoring of fat supplies.
Fat cells produce a peptide (leptin), which signals the brain to increase or decrease eating. (Leptin receptors have been identified throughout the hypothalamus)
Low levels of leptin increase hunger
High levels reduce eating and increase physical and immune system activity
Arcuate nucleus
Receives information from all parts of the body regarding hunger.
Master area for controlling appetite.
Contains two sets of neurons:
NPY neurons: appetite increasing neurons (hungry)
POMC neurons: appetite suppressing neurons (full)
Hunger signals
Appetite increasing neurons receive information from multiple sources to increase hunger. (NPY neurons)
Ghrelin:
Released from the stomach into the bloodstream
Crosses blood-brain barrier to influence the hypothalamus
May be produced by the hypothalamus itself
Ghrelin release is inhibited by leptin
Satiety signals
Input to appetite suppressing neurons (POMC/full neurons) of the arcuate nucleus include:
Signals of both long-term and short-term satiety.
Distention of the intestine triggers neurons to release the neurotransmitter CCK.
Blood glucose levels
Leptin release from body fat
Paraventricular nucleus
Output from the arcuate nucleus goes to anorexigenic neurons in the paraventricular nucleus of the hypothalamus.
Axons from the satiety-sensitive cells of the arcuate nucleus deliver excitation to the paraventricular nucleus.
Causes release of melanocortins which limit food intake.
Full pathway.
The lateral hypothalamus
Receives input from both POMC and NPY neurons of the arcuate nucleus:
Inhibition from appetite surprising POMC neurons.
Excitation from appetite stimulating NPY neurons.
Stimulation of the orexigenic neurons in the lateral hypothalamus increases the drive to eat.
Hungry pathway.
