PSYC 2410 Chapter Notes - Chapter 12: Blood Sugar, Glycogen, Insulin

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19 Apr 2012
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BEHAVIOURAL NEUROSCIENCE Week 9
Chapter 12- Hunger, Eating and Health
12.1- Digestion, Energy Storage, and Energy Utilization
Digestion- is the gastrointestinal process of breaking down food and absorbing its constituents into the
body
E is delivered to the body in 3 forms: lipids, amino acids and glucose
- E is used continuously but its consumption is intermittent therefore the body stores E (in the form of:
fats, proteins and glycogen) between meals. The body stores mostly fat and little of proteins and
glycogen
Why is fat the body’s preferred way of storing E?
- a gram of fat can store almost twice as much energy as a gram of glycogen
-glycogen, unlike fat, attracts and holds substantial quantities of water
3 Phases of Energy Metabolism
1. Cephalic Phase- preparatory phase; often begins with the sight, smell of thought of food, and it ends
when the food starts to be absorbed into the bloodstream
2. Absorptive Phase- the E absorbed into the bloodstream from the meal is meeting the body’s
immediate E needs
3. Fasting Phase:- all of the unstored E from the previous meal has been used and the body is
withdrawing E from its reserves to meet its immediate E requirements; it ends with the beginning of the
cephalic phase
-(rapid) weight can likely arises when a person frequently skips of the fasting phase
2 Pancreatic hormones: insulin and glucagon
- control the flow of E during the 2 phases of E metabolism
Cephalic & Absorptive
- pancreas releases a lot of insulin into the bloodstream and a little bit of glucagon
Insulin
1. Promotes the use of glucose as the primary source of E by the body
2. Promotes the conversion of blood-borne fuels to forms that can be stored: glucose to glycogen and
fat, and amino acids to proteins
3. Promotes the storage of glycogen in liver and muscle, fat in adipose tissue, and proteins in muscle
Fasting
-characterized by high levels of glucagon blood levels and low levels of insulin
-w/o high levels of insulin, glucose has difficulty entering most body cells; thus glucose stops being the
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body’s primary fuel source
- this saves the body’s glucose for the brain, because insulin is not required for glucose to enter most
brain cells.
-the low levels of insulin also promote the conversion of glycogen and protein to glucose
(gluconeogenesis- conversion of protein o glucose)
-high levels of fasting-phase glucagon promotes the release of free fatty acids from adipose tissue and
will be used as the body’s primary fuel source. Free fatty acids are also converted into ketones, which
are used by the body’s muscles through the fasting phase
-the brain will begin to use ketones after a prolonged period of fasting
12.2 Theories of Hunger and Eating: Set Points vs. Positive Incentives
Set-point Assumption- after a meal, a person’s E resources are assumed to be near their set point and
to decline thereafter as the body uses E to fuel its physiological processes. When the level of the body’s
E resources falls far enough below the set point, a person becomes motivated by hunger to initiate
another meal. The meal continues, according to the set-point assumption, until the E level returns to its
set point and the person feels satiated (no longer hungry)
All set point systems have 3 components:
1. Set-point Mechanism- defines the set point (ex. Thermostat)
2. Detector Mechanism- detects deviations from the set point (ex. Thermometer)
3. Effectors Mechanism- acts to eliminate the deviations (ex. Heater)
- All set points are negative feedback systems- systems in which feedback from changes in one
direction elicit compensatory effects in the opposite direction; act to maintain homeostasis- a
stable internal environment
Glucostatic and Lipostatic Set-Point Theories of Hunger and Eating
Glucostatic Theory- eating regulated by a system that is designed to maintain a blood glucose set-
pointthe idea being we become hungry when our blood glucose levels drop significantly below their
set point and that we become satiated when eating returns out blood glucose levels to their set point
Lipostatic Theory- every person has a set-point for body fat, and deviation from this set point produce
compensatory adjustments in the level of eating that return levels of body fat to their set point. A
support to this theory is the fact that the body weights of adults stay relatively constant
*the GT was thought to account for meal initiation and termination, whereas the LT was through to
account for long-term regulation
Problems with Set-Point Theories of Hunger and Eating
-there is an epidemic of obesity and overweight, which should not occur if eating is regulated by a set
point
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Positive-Incentive Perspectives (PIP)
Positive-incentive Theory- humans and other animals are not normally driven to eat by internal E
deficits but are drawn to eat by the anticipated pleasure of eatingthe anticipated pleasure of a
behaviour is called its positive-incentive value
-acknowledges that many factors interact to determine a person’s hunger at any time
According to the PIP, it is the presence of good food, or the anticipation of it, that normally makes us
hungry, not an E deficit. The degree of hunger you feel at any particular time depends on the interaction
of all the factors that influence the positive-incentive value (ex. Flavour, the effects you have learned
about the food, last time you ate until now, quantity and type of food already in your gut, etc)
12.3 Factors That Determine What, When, and How Much We Eat
Factors That Determine What We Ea
-certain tastes have a high +ve incentive value for virtually all members of a species (ex. Sweet, fatty,
and salty for humans)
-bitter tastes, for which humans have an aversion, are often associated with toxins
Learning to Eat Vitamins and Minerals
2 patterns:
1. Sodium- when an animal is deficient in sodium, it develops and immediate and compelling preference
for the taste of sodium salt
2. Essential Vitamins- when an animal is deficit in some vitamin or mineral other than sodium, it must
learn to consume foods that are rich in the missing nutrient by experiencing their positive effects
Factors That Influence When We Eat
-most animals eat many small meals if there is a continuous access to a food source
-many people experience malaise (headache, nausea, and inability to []) when they miss a regularly
scheduled meal
Pre-meal Hunger
-According to Woods, the key to understanding hunger is to appreciate that eating meals stresses the
body. Before a meal, the body’s E reserves are in reasonable homeostatic balance; then, as a meal is
consumed, there is a homeostatic-disturbing influx of fuels into the bloodstream.
-the cephalic phase prepares for the homeostatic disturbance by releasing insulin and reducing blood
glucose. Mealtime hunger is caused by the expectation of food, not by an E deficit
Factors That Influence How Much We Eat
Satiety- a motivational state that causes us to stop eating a meal when there is food remaining
-food in the gut and glucose entering the blood can induce satiety signals. These signals depend on
volume and nutritive density
Nutritive Density-calories per unit volume
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