Hunger and Thirst

homeostasis

process by which the body’s substances and characteristics are maintained at their optimal level

system variable

variable controlled by a regulatory mechanism

set point

optimal value of the system variable in a regulatory mechanism

detector

mechanism that signals when the system variable deviates from the set point

correctional mechanism

mechanism that is capable of changing the value of the system variable

negative feedback

process whereby the effect produced by an action serves to diminish or terminate that action

give an example of a negative feedback loop (heater)

detector —> thermostat

temperature setting —> set point

air temperature —> system variable

electric heater —> correctional mechanism

when the air temperature drops and the thermostat reading drops below the thermostat setting, the heater will turn on and warm the air, providing a negative feedback to return the temp back to the appropriate setting

ex. of negative feedback (drinking water)

1. body loses water

2. detector signals loss of water

3. drinking occurs (correctional mechanism)

4. stomach fills with water, sends signal to brain (brain regions making you thirsty will shut down to ensure you aren’t drinking too much water)

5. satiety mechanism inhibits further drinking

6. water is absorbed; body fluids go back to normal

intracellular fluid

fluid contained within cells

extracellular fluid

all body fluids outside cells

intravascular fluid

fluid found within blood vessels

interstitial fluid

fluid that bathes the cells, filling the space between cells of the body

isotonic

equal in osmotic pressure to the contents of the cell

how much of the body is intracellular fluid

67%

how much of the body is interstitial fluid

26%

how much of the body is intravascular fluid

7%

how much of the body is cerebrospinal fluid

less than 1%

what comprises extracellular fluid

interstitial fluid, intravascular fluid (blood plasma), cerebrospinal fluid

if solution A is hypertonic to solution B, where is water going

drawn out of B and going into A

if solution C is hypotonic to Solution B, where is water going

going out of C and into B

osmometric thirst (osmotic)

thirst produced by an increase in the osmotic pressure of the interstitial fluid relative to the intracellular fluid

osmoreceptor

neuron that detects changes in the solution concentration of the interstitial fluid that surrounds it

water loss through evaporation

1. water is lost through evaporation

2. concentration of interstitial fluid increases

3. capillaries and cells lose water by osmosis

what happens as salt concentration of interstitial fluid increases?

water leaves the cell, and the cell decreases in volume. Change in cell volume triggers a change in firing rate, which signals thirst or satiety 

what happens as salt concentration of interstitial fluid decreases?

water enters the cell and the cell increases in volume. change in cell volume triggers a change in firing rate, which signals thirst or satiety

circumventricular organs

specialized regions of the brain with rich blood supply located along the ventricular system

• OVLT and SFO

OVLT

organum vasculosum of the lamina terminalis, lacks a blood brain barrier, most osmoreceptors are located here

SFO

subfornical region, some osmoreceptors here

what does damage to circumventricular organs cause

adipsia — lack of drinking

vasopressin

hormone released by posterior pituitary which raises blood pressure by constricting blood vessels

• helps to compensate for the decreased water volume 

• also involved in reproductive behaviors

• inhibited by alcohol

why is vasopressin known as an antidiuretic hormone

enables the kidneys to reabsorb water and excrete highly concentrated urine

volumetric thirst

thirst produced by hypovolemia

hypovolemia

reduction in the volume of intravascular fluid —loss of blood, vomiting, diarrhea

renin

hormone secreted by the kidneys that cause the conversion of angiotensinogen to angiotensin II

angiotensin II

peptide hormone that constricts blood vessels, causes the retention of sodium and water, and produces thirst and a salt appetite

how does body detect hypovolemia

SFO contains neurons that detect the presence of angiotensin in the blood and excites neural circuits initiating drinking

explain sequence of fixing hypovolemia

reduced blood flow to kidneys —> renin converts angiotensinogen to angiotensin 1 —> angiotensin 2 —> 2 causes retention of sodium and water, increasing blood pressure, creating a salt appetite and drinking

osmotic thirst stimulus

high solute concentration outside cells causes loss of water from cells

osmotic thirst best relieved by drinking…

water

osmotic thirst receptor location

OVLT, a brain area adjoining the third ventricle

osmotic thirst hormone influences

accompanied by vasopressin secretion to conserve water

hypovolemic thirst stimulus

low blood volume

hypovolemic thirst best relieved by drinking

water containing solutes

hypovolemic thirst receptor location

1. receptors measuring blood pressure in the veins

2. subfornical organ, a brain area adjoining the third ventricle

hypovolemic thirst hormone influences

increased by angiotensin II

median pre-optic nucleus

• OVLT, SFO, and nucleus of the solitary tract connect to this

• output of this drives drinking behavior

feast or famine hypothesis

before agriculture, drive is to eat as much food as possible when it’s available because they would go awhile without food

• need carbohydrates, fats, amino acids, vitamins, and minerals

• need to balance food availability, metabolism, body weight, and nutrition

• body needs to store nutrients for use when animal is not filling stomach (carbs is short term, fats is long term)

glucose

source of energy for the body and nearly the only fuel used by the brain, most digested food enters the bloodstream as this

what happens when glucose levels are high

the liver converts some of the excess into glycogen and fat cells convert it into fat

what happens when glucose levels are low

liver converts glycogen back into glucose

when do insulin levels rise?

• rise as someone is getting ready for a meal, and after a meal

• high levels of insulin generated during a meal generally decrease appetite

what happens when there is extra insulin in the body

it’s a satiety signal to turn glucose into glycogen

what happens during famine

glucagon is produced and turns glycogen into glucose

explain the insulin and glucagon negative feedback loop (when blood glucose rises)

1. beta cells release insulin into blood by pancreas

2. body cells take up glucose/liver takes glucose and stores it as glycogen

3. blood glucose declines

explain the insulin and glucagon negative feedback loop (when blood glucose falls)

1. alpha cells in pancreas release glucagon

2. liver breaks down glyocogen and releases glucose

3. blood glucose levels rise 

mechanism 1 of stomach control of eating

1. distension sensed by stretch receptors

2. sent as signal to the brain by vagus nerve

3. satiety

mechanism 2 of stomach control of eating

1. release of cholecystokinin

2. closes muscle between stomach and duodenum

3. reduces gastric emptying and stomach distends faster

mechanism 3 of stomach control of eating (ghrelin secretion)

• stimulates hunger (the level of this increases before a meal)

• ghrelin from stomach and digestive track signals the hypothalamus

• stimulates hunger/feeding

constant high ghrelin level causes…

prade-willi syndrome (constant eating, obesity)

what starts a meal?

metabolic signals —> glucoprivation, lipoprivation

• the liver has sensory neurons that sense decreased glucose and send a message to brain via the vagus nerve

glucoprivation

dramatic fall in the level of glucose available to cells

lipoprivation

dramatic fall in the level of fatty acids available to cells

what do the brain and body use for energy

brain uses glucose only, rest of the body cells use both glucose and fatty acids

nutrient receptors

receptors for glucose and lipids are located in the liver and convey signal about gluco and lipoprivation to the brain through the vagus nerve

glucose detectors in brain

brain cannot metabolize fatty acids; receptors detect only glucose levels

glucose and lipid detectors in liver

• liver can metabolize glucose and fatty acids, receptors detect levels of both nutrients 

• signal to brain via vagus nerve to start a meal when nutrients are low 

long term satiety

signals from adipose tissue

leptin

• hormone secreted by adipose tissue that may be involved in long term satiety

• more fat = more leptin

• low levels of leptin increase hunger

lateral hypothalamus and hunger

regulates hunger, motivation to find food

arcuate nucleus and hunger

controls how the LH responds

ventromedial hypothalamus and hunger

responsible for satiety 

feeding circuits in brain

MCH and orexin in lateral hypothalamus excite thalamus, reticular formation, locus coeruleus, periaqueductal gray matter, and neurons in spinal cord that control the ANS

brain regions involved in causing hunger

• as ghrelin levels go up, NPY activity in arcuate nucleus goes up, and feeding behavior increases 

• NPY/AGRP excites MCH and orexin in lateral hypothalamus, causing excitatory effects on eating, reduction of metabolic rate 

what in the brain causes satiety

• NPY neurons are inhibited, and CART neurons are excited

• CART/alpha-MSH inhibit MCH and orexin in LH, paraventricular nucleus

• leptin secretion by adipose tissue indirectly inhibits paraventricular nucleus

• PYY released in stomach, and the more the stomach distends, the more PYY released, inhibiting NPY/AGRP