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Lecture 16

PSYCH 1XX3 Lecture Notes - Lecture 16: Opioid Receptor, Adipose Tissue, Leptin


Department
Psychology
Course Code
PSYCH 1XX3
Professor
Joe Kim
Lecture
16

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Lecture 16: Hunger and the Chemical Senses
Introduction to Hunger and Satiety
Seeking out food and drink is a fundamental goal-directed behaviour because your
moving body needs regular nourishment to function optimally
During most of the human evolutionary past, food sources were scarce and behaviours
were motivated by the constant need to obtain energy and nutrients essential for
survival
Feeding behaviours may be motivated by hunger and satiety signals, but are guided to a
large extent by the interaction of the senses of taste and smell
Hunger and Satiety
Overnight, you have fasted for the longest period of your daily cycle
Many signals and complex interactions between the brain and digestive system that
drive your feelings of hunger to consume food and drink and satiety signals which lead
you to stop consumption
Glucose and Glycogen Balance
o When you are fasting, one of the main reasons you feel hungry is low blood
glucose levels
o Glucose is important for keeping your body’s functions operating and is the
preferred source of energy for the brain
o Unlike other organs and tissues, the brain cannot use fat energy stores for fuel,
which makes regulating glucose levels a top priority
o You are very sensitive to the level of glucose in your blood and this directly
relates to your feelings of hunger
o To keep your brain constantly supplied with energy, your body can store glucose
in the form of glycogen, which can be released in between meals
o Some glycogen is stored in the muscles, but the main supply is in your liver
where it can be readily converted back into glucose when your circulating blood
glucose levels are low
o This glucose-glycogen balance is mediated to a large degree by the liver and a
pancreatic hormone called insulin
o After a meal, the pancreas secretes insulin to promote the uptake of glucose by
cells in your body for immediate use, but also to stimulate storage of excess
glucose as glycogen
o As time goes by, your blood glucose levels will correspondingly begin to dip
o When these levels get low enough, the liver begins to breakdown its stored
glycogen into glucose, releasing it back into circulation
o In this way, liver and pancreas help to buffer extreme swings in blood glucose
levels
o As this cycle continues and the time since your feast increases, your glycogen
reserves in the liver will decrease and a status signal is sent to the brain
o At some point, the glucose and glycogen levels get too low and you will feel
hungry

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o In the time between a meal and the next morning, your glycogen stores are
being depleted
o Eating a bowl of cereal increases your blood glucose levels for now and helps to
replenish your glycogen stores for later
NPY
o Another hunger cue you were likely to experience this morning came from
Neuropeptide Y (NPY)
o High levels of NPY activity in the hypothalamus are associated with increased
appetite and food seeking behaviours (ex. heading to the kitchen)
o NPY affects feeding behaviour similarly in fish, reptiles, birds and other non-
human mammals
Satiety and the Liver
o Just as your liver and send signals to your brain to trigger hunger, it can also send
signals to the brain that trigger satiety
o Ex. If you take a dog that is eating and you inject glucose into a vein that
connects directly to the liver, the dog will stop eating
o However, when the same glucose dose is injected into a different vein, such as
one that does not connect to the liver, the dog will continue eating
o The liver monitors glycogen stores and blood sugar levels
o Low blood glucose and low glycogen levels serve as signals of hunger, while high
glucose levels and high glycogen stores are signals of satiety
CCK and Meal Duration
o The small intestine also has a role to play in feelings of satiety
o As your breakfast moves from your stomach to your gut, the small intestine
produces Cholecystokinin (CCK), a hormone that is responsible for feelings of
satiety or fullness after a meal
o Receptors in the brain detect CCK, which serves as a signal to stop eating
o Scientists have found that if you inject individuals with CCK, they report feeling
satiated sooner
o In another study, researchers administered CCK to rats leading to shorter than
average meal durations compared to controls
o Interestingly, these rats who received CCK ate more total meals per day than the
controls and so the total daily food intake was actually the same for both
groups
o This shows that CCK is a short-term satiety signal
o CCK appears to regulate short-term feeding behaviours, but not long-term
energy consumption
Long-Term Weight Regulation
Animals need to consider more than their current nutritional needs, they also need to
store some excess energy for use in times when food is scarce
Whenever possible, long-term energy storage takes place in the form of fat (adipose
tissue)
Both short-term and long-term mechanisms interact to regulate overall energy balance
and body-weight

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Adipose Energy Stores
o Why do animals store most of their excess energy in the form of fat instead of
storing it all as glycogen, which is a quickly transferable source of energy
o For one thing, fat has more than twice the energy that carbohydrates like
glycogen have
o For every 1 gram of fat, there are 9 units of kilocalories, while carbohydrates
only contain 4 kilocalories per gram
o Unlike glycogen, fat is found in virtually all parts of the body
o For the long term, fat is a better choice for storing more energy
o But fat or adipose tissue is more than just a passive energy storehouse
o It is an active component of your regulatory physiology and was fairly recently
classified as an endocrine organ as well
Leptin
o Adipose tissue secretes a hormone called leptin, which is involved in long-term
energy balance and correlated with fat mass
o When leptin levels rise, they act on receptors in the hypothalamus to reduce
appetite and consequently, food consumption decreases
o Leptin production is controlled by the OB Gene
o In genetically altered knock-out mice lacking an OB Gene, leptin production
stops
In this state, mice are missing a key hormonal signal to regulate appetite
and become extremely obese
This condition can be reversed if mice are given regular injections of
leptin, causing their eating behaviour and weight to return to normal
o These studies suggest that a contributing factor for obesity in humans may
involve defective OB genes or receptors
o This inference is not supported in clinical findings however
o If you were to give an obese animal who has normal leptin levels additional
leptin, there is no weight loss to return leptin levels to normal
o It appears that humans and other animals are capable of becoming leptin
resistant
Beyond a certain point, leptin’s ability to inhibit appetite is reduced
o For most of evolutionary history, access to calories was a limited resource for
humans
o It is more than likely that the primary adaptive function of leptin was to serve as
a n indicator of low energy stores, rather than as a signal to directly reduce food
intake
o Low levels would signal to increase foraging effort or minimize activity in order
to conserve energyfv
o Rarely would an individual have very high levels of leptin suffer from negative
effects associated with excess adipose tissue
NPY
o Leptin acts to inhibit the actions of NPY
o NPY mediated increase in appetite is prevented by leptin, leading to decreased
appetite and energy consumption
o Together, leptin and NPY interact to regulate weight to optimal levels
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