Lecture 17 Flashcards
Homeostasis
Body’s characteristics like temp and glucose level are maintained at their optimum level
Ingestive behavior
eating or drinking
Physiological regulatory mechanisms (3)
System variable - variable controlled by a regulatory mechanism (like temp is controlled by a heating system)
Set point - Optimal value of the system variable in a regulatory mechanism
Correctional mechanism - In regulatory process, the mechanism that is capable of changing the value of a system variable
Physiological regulatory mechanisms (2)
Negative feedback - the effect produced by a correctional mechanism serves to diminish the corrective action
Satiety Mechanism - Brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water
Water negative feedback (6 steps)
1 body loses water therefore body fluid low
2 detectors signal loss of water
3 drinking occurs
4 stomach fills with water, signals brain -> 5a and 5b
5a satiety mechanism inhibits further drinking
5b water is absorbed, body fluid goes back to normal
5a INHIBITS 3
Body fluid compartments
67% pf water is stored as intracellular fluid
26% as extracellular fluid
7% as intravascular fluid (blood plasma)
1% or less - CSF
Thirst occurs when (2 things)
(1) there is not enoigh blood circulating - Volumetric thirst
(2) there is too much salt in the blood (osmometric thirst)
Volumetric thirst basics
Occurs when there is not enough blood circulating
Hypovolemia causes volumetric thirst: this is why people feel thirst after blood loss
Blood flow is monitored by the kidneys. Low blood flow causes renin release. This causes a hormone cascade which activates hypothalamic neurons in the anteroventral tip - the AV3V region where the blood brain barrier is weak
Volumetric thirst cascade
Hypovolemia
Reduced blood flow to kidneys
Renin - converts angiotensin 1 to angiotensin 2
Angiotensin 2 promotes
- Retention of sodium
- Retention of water
- Increase in BP
- Salt appetite
- Drinking
Osmometric thirst and tonicity
Tonicity is the relative concentration of dissolves solutes on either side of a semipermeable membrane. It is used to describe the direction and extent across the membrane of water movement (osmosis)
Isotonic - equal solute concentrations, no net flow of water
Hypotonic solution - solute is less concentrated outside than in so water enters cell
Hypertonic solution - solute is more concentrated outside cell than in so water will leave the cell
Osmoreceptors
Hypertonic solutions cause cell dehydration
Osmoreceptors are neurons that detect changes in cell size which corresponds to the interstitial solute concentration. The membrane potential and release of neurotransmitter from osmoreceptor cells relates to the volume of these cells
Osmometric thirst
Some neurons of the Av3V region of the hypothalamus are osmoreceptors
Ingestion of hypertonic saline activates neurons in the Av3V region and the anterior cingulate cortex
Drinking water immediately quenches activity in the anterior cingulate cortex. So there IS a rapid feedback system.
BUT Av3V neurons mostly remain active if their osmoreceptor proteins remain active
Cold sensors in mouth and sensory fibers in the stomach are part of the rapid feedback system. When these firs the activity in the anterior cingulate cortex drops off.
Insulin/Glucagon and sugar
Pancreases detects blood glucose. When high, releases insulin which causes muscle and liver cells to store glucose as glycogen.
Cells internalize glucose with a transporter that only works with insulin present EXCEPT the brain which has another transporter that always works
This means cells outside the brain can only use glucose when there is excess around (and hence, insulin). Without this, they must use fatty acids.
A drop in blood glucose causes the stopping of insulin release. This means that most cells cannot use glucose. This reserves glucose in the blood for the CNS
Insulin
Homone
1 - glucose to glycogen
2 - entry of glucose and AAs into cells
3 - Transport fat into adipose cells
Glucagon
Hormone
1 - Conversion of liver glycogen into glucose
2 - Conversion of adipose triglycerides into fatty acids
Troiglyceride
Glycerol + 3 fatty acids
The liver can convert glycerol into sugar
Cells outside the brain can turn fatty acids into sugar
Stomach signals
An empty duodenum is communicated to the bran by release of ghrelin
Levels of this increase with hunger and fall with satiation
Exogenous administration of ghrelin increases hunger and food intake
BUT decrease of it does not stop hunger, just decreases big meals and makes small, snack like meals more likley
What starts a meal
Ghrelin released by empty stomach increases eating
Regulated by presence or absence of ghrelin from the stomach
What stops a meal
Short term satiety signals are released after eating and before digestion (NOT swelling of the stomach)
Cholecystokinin (CCK) and PYY are secreted by the duodenum in proportion to calories ingested. They correlate with feelings of fullness but inhibit food intake. They are short lived and mostly influence how long we eat for.
(CCK also regulates gastric motility and cases digestive enzyme release by the gallbladder).
Administration of CCK and PYY does not lead to weight loss. It causes lower meal size but the body reacts with more meals.
Ghrelin, CCK and PYY regulate
MEAL TIME HUNGER
After a meal
The satiety produced by CCK and PYY is anticipatory, your cells have not yet received the nutrients
Not until nutrients are absorbed can they be used as fuel
This stage is signaled by the liver and pancreas as they detect when food has been absorbed into the blood and available to the body
The liver measures glucose and FAs in the blood and signals through the Vegas nerve
The pancreas measures glucose and releases blood insulin which is actively transported across the BBB. The detection of insulin by the hypothalamus reduces hunger
Long term satiety signals (adipose tissue)
If an animal is force-fed it will reduce its food intake when it is allowed to do so
Body weight is regulated in most people over a long term period
Leptin
Secreted by adipocytes
Signals size of peripheral energy store
More fat = more leptin = lower hunger
Exogenous leptin administration drops meal size temporarily in healthy people
Leptin deficiency causes massive obesity, resolved with administration of exogenous leptin
Emergency hunger citrcuits
Glucoprivation
Low glucose available to cells. Detected in brainstem and liver
Can be caused by excess signaling or drugs that inhibit glucose metabolism
Often caused by insulin misuse
Lipoprivation
Low fatty acid level detected in liver and brain
Usually caused by drugs that inhibit FA metabolism but could also be with too little bodyfat
