Midterm 3 (Final) Chapter Notes P2.pdf
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PSYC211 Chapter 12 Notes
Carrie was nursed poorly and she was thus underweight. Her motor and cognitive development had also been slow. Eventually, she
regained her appetite and had put on some weight. She soon became heavier than she should be at her age and had developed
compulsive behaviour: skin picking, collecting and lining up objects etc.
She also had a problem eating. She would eat everything she could get her hands on at school and at home. From her designated
meals to leftovers to pieces of scrap food thrown into the garbage.
A specialist diagnosed her condition and limited her caloric intake to 1200 calories a day. She was appointed a monitor to keep her
on track at school.
Carrie has been diagnosed with Prader-Willi syndrome caused by a deletion of several genes on chromosome 15 that are involved
in the production of proteins that regulate the functioning of the hypothalamus. This is caused by random accidents in the production
of sperm cells.
For an organism to live in a possibly hostile environment it needs a barrier between its cells and the environment. Within this barrier,
the internal ﬂuid of the cell has to be regulated.
For this regulation, known as homeostasis, to occur, we have digestive, respiratory, circulatory and excretory systems.
Physiological Regulatory Mechanisms:
Physiological regulatory mechanism: keeps constancy in the cell while the exterior of the cell face variability. EX: constant body
temperature while exterior temperature changes.
4 features of a regulatory mechanism:
1. System variable: the characteristic that is being regulated EX: temperature
2. Set point: the optimum value of the system variable, the value we want to regulate to EX: 37°C
3. Detector: device that monitors and signals when the system variable deviates from the set point.
4. Correctional mechanism: mechanism that will restore the system variable to the set point.
Example: room regulated by thermostatic heater- Figure 12.1.
System variable: the air temperature of the room
Set point: preset value for the desired temperature
Correctional mechanism: the coils of the heater
Negative feedback: the effect produced by an action serves to diminish or stop that action. EX: the heater turns on to increase the
temperature, but turns off shortly after because it has felt the increase in heat.
Eating and drinking are correctional mechanisms that replenish the body’s water and nutrient supplies. These ingestive behaviors
are controlled by satiety mechanisms (cessation of hunger or thirst). Satiety mechanisms monitor the correctional mechanisms and
not the actual system variables because it takes time for ﬂuid that is just ingested to replenish the system variable. Figure 12.2
Summary p. 408-409.
Eating: Some Facts About Metabolism
Water balance can be achieved by the intake of two ingredients: water and sodium chloride.
When we eat, we must ingest enough carbohydrates, fats, amino acids, vitamins and minerals (not sodium). Eating is more
complicated than drinking.
Control of eating: metabolism, regulation of body weight, environmental and physiological factors that begin and stop a meal and the
neural mechanisms that monitor the nutritional state of our bodies and control our ingestive behaviour.
Eating disorders: obesity and anorexia nervosa.
Why do we eat? We eat to construct and maintain our own organs and obtain energy for muscular movement and body heat.
Building blocks and fuel.
Our cells needs fuel and oxygen to stay alive, however our stomachs are sometimes empty. We have two reservoirs that save our
nutrients: short-term (carbohydrates) and long-term (fats).
•in the liver cells and muscles
•ﬁlled with complex, insoluble carbohydrate: glycogen
•in the liver: convert glucose to glycogen and store it with the presence of insulin (peptide hormone). When all the glucose
is either used as fuel or converted into glycogen, the glucose blood level falls and the pancreas and the brain detect this
fall. Pancreas’ response: stop secretion of insulin, start secretion of glucagon which turns glycogen into glucose. Liver’s
response: soak up the excess glucose and store it as glycogen and the cycle repeats itself.
•Reservoir used for the CNS: your brain is fed by your liver which converts glycogen to glucose and sends it into the blood
stream. The neurons and the glia absorb and metabolize it. When there is not enough glucose, we usually eat more. If
we don’t, the brain taps into the long-term reservoir.
Only pages 1-3 are available for preview. Some parts have been intentionally blurred.
•Adipose tissue: fat tissue- triglycerides: contain glycerol and three fatty acids
•Found beneath the skin and the abdominal cavity
•Able of absorbing nutrients from the blood and converting them to triglycerides to store them.
•The cells can expand to an abnormally enormous size= giant fat cells.
•Keeps us alive when we are fasting: fat cells convert triglycerides into fuel
•When the brain uses the short term reservoir, the other parts of the body use the fat tissue. The reason why the other
body parts leave the liver glucose to the brain is because glucose doesn’t dissolve well in fatty tissues. That means they
need a transporter to get them through the double fat layer of cell membranes. There are insulin receptors on these
glucose transporters. There needs to be insulin so that glucose can enter a cell. The exception to this rule is the cells in
the nervous system that don’t have insulin receptors on the transporters. Glucose can use the transporters in any
condition to enter the cells. Figure 12.12
Fasting phase: metabolism that occurs when no food is available from the digestive system: when glucose, amino acids
an fatty acid are derived from glycogen, protein and adipose tissue.
Absorptive phase: metabolism that occurs when food is available from the digestive system. Glucose and amino acids
are used up in this phase.
EX: balanced meal of proteins, carbohydrates and fats.
proteins→ amino acids
1. Absorb nutrients, blood glucose increases. The rise is detected by brain cells which causes the activity of the
sympathetic nervous system to decrease and the activity of the parasympathetic nervous system to increase.
This cause the pancreas to stop secreting glucagon and start secreting insulin. Glucose can now be used as
fuel. The extra glucose is converted into glycogen and is stores in the short-term reservoirs. The glucose left
over is stored as fat cells in the long-term reservoir.
2. Some amino acids are used as building blocks and the rest are converted into fat.
3. Fats are stored in the long-term reservoir as adipose tissue.
Summary p. 412.
What Starts a Meal?
Regulation of body weight: balance between food intake and energy expenditure.
If energy expenditure is constant, 2 mechanisms needed for control:
1. Increase motivation to eat if the long-term reservoir is being depleted
2. Restrain food intake if we eat more calories than we need.
Signals from the Environment:
Over-eating is a biological, evolutionary activity. For our ancestors over-eating when there was a lot of food assured they had
enough in their long-term reservoirs to keep them healthy when food became scarce.
An empty stomach is the most obvious signal, but there are psychological reasons why people eat (hearing its time to eat, seeing
the time that you usually eat at, etc.)
Signals from the Stomach:
The gastrointestinal system releases a peptide hormone ghrelin: controlling the release of the growth hormone. Ghrelin increased
with fasting and decreased with a large meal. Blood levels of ghrelin increase right before a meal.
As Ghrelin increases, food intake increases (hunger). Figure 12.13
Probable cause of over-eating: chronic elevation in the blood level of ghrelin (it will stay high even after a meal).
The most common obesity surgery: gastric bypass operation that suppresses ghrelin secretion.
The release of the hormone in normal organisms is controlled by the contents of the digestive system (mostly the upper part of the
small intestine) and not by the availability of nutrient in the blood.
Ghrelin is not the only reason though, because even after the gastric bypass surgery was successful and there is almost no ghrelin
in the blood, people still had the compulsion to eat food, indicating that there is another activator of hunger.
We get hungrier and hungrier after not eating consecutive meals because there is a physiological signal that is telling us we are
tapping into our long-term reservoir.
Only pages 1-3 are available for preview. Some parts have been intentionally blurred.
During the absorptive phase of metabolism, we live of food that is being absorbed through our digestive tract. After that phase, we
start absorbing food from our reservoirs: brain gets glucose, rest of body gets fatty acids. This is when we need to start thinking of
our next meals.
A potent signal of hunger is a fall in blood glucose level= hypoglycemia causing glucoprivation (fall in level of glucose available to
Lipoprivation (depriving cells of the ability to lipids) also causes hunger.
There are two sets of receptors that the level of metabolic ﬂuid:
1. Located in the brain: monitor the nutrients on its side of the blood brain barrier- sensitive to glucoprivation
2. Located in the liver: monitor the rest of the body- sensitive to glucoprivation and lipoprivation
Summary p. 415.
What Stops a Meal?
Two satiety signals (signals that stop a meal).
1. Short term satiety: immediately after eating (long before digestion).
2. Long-term satiety: arise in adipose tissue (long-term reservoir).
These signals control the long-term intake of calories.
The consequences of starvation are worse that the consequences of over-eating so natural selection has selected stronger
characteristics of our bodies that signal when we are hungry rather than when we are overly full.
If there was a strong inhibitory control of eating, then it would be hard to make people eat more than they should.
People eat a larger meal is the food is tasty, eaten with other people and if the meal is latet in the day: environmental factors.
Receptors located in the head: eyes, nose, tongue and throat. Info about appearance, smell, taste, texture and temperature of food
have automatic effects on intake.
However, the mere act of eating will not cause satiety because people who have gastric ﬁstula (a tube that drains food out of the
stomach before digestion) can eat indeﬁnitely.
Learning about the food we eat will lessen our eating habits: taste and odor affect our learning about caloric intake the most. EX:
people were full when they knew the soup was high in fat even though scientists were able to infuse more than the eaten amount
into their stomachs using a ﬂexible tube.
The stomach contains receptors that detect nutrients. EX: rats ate to their full and then researchers emptied their stomachs and let
the rats eat again. The rats ate the same amount of food as the ﬁrst time which implies that the stomach knows if its full or not.
Intestines contain nutrient detectors. EX: in rats, efferent axons arising from the duodenum are sensitive to the presence of glucose,
amino acids and fatty acids. These axons can transmit satiety signals to the brain.
Intestinal factors in humans: EX: a groups of people swallowed a bag that can be ﬁlled with air by the attached tube. When the
stomach and duodenum was empty and the bag was ﬁlled with air, the subjects said they were hungry but bloated. When fats and
carbohydrates were infused at the same time as the bag was being ﬁlled with air, subjects said they were full.
When food reaches the stomach it is attacked by hydrochloric acid and pepsin which break proteins into their amino acids. As
digestion proceeds, food is introduced into the duodenum where it continues to be digested by bile and pancreatic enzymes.
Cholecystokinin (CCK) controls the rate at which food leaves the stomach and enters the duodenum. CCK levels are proportional to
levels of nutrients the duodenum receives. This could be sending signals to the brain of satiety via the vagus nerve. EX: injections of
CCk induce satiety.
The chemical peptide YY3-36 (PYY) is released after nutrient intake in proportional amounts to the caloric intake. PYY has decreased
the size of meals eaten. Figure 12.16
Gastric factors and duodenal factors are anticipatory: predicting the food that has been eaten will restore the depleted reserves.
EX: glucose and fructose are injected into the hepatic portal vein in the same amount as when food is being digested. This caused
the rats to eat less by “fooling” the liver. Fructose is easiest metabolized in the liver which means the signals of satiety felt by the
rats must be from the liver. So, when the liver receives nutrients from the intestines it sends extra satiety signals to the brain.
Absorptive phase of metabolism is accompanied by an increased level of insulin which will metabolize the glucose and allow
triglycerides to enter fat cells. The brain doesn’t need the insulin to metabolize glucose though, however, the brain does have
glucose receptors. Why?
They detect when insulin is in the blood and this tells the brain that the body is probably in the absorptive phase of metabolism.
Also, a transport mechanism brings insulin to the brain and it reaches the neurons in the hypothalamus which control eating and
hunger. Insulin is infused into the third ventricle and this inhibits eating and causes a loss of body weight.
Long-term Satiety: Signals from Adipose Tissue:
The previous are all short term effects of eating a single meal.
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