Psych 1XX3 – Hunger and Chemical Senses Notes – Mar 26, 2010
Human evolutionary past: food sources were scarce and behaviours were
motivated by the constant need to obtain energy and nutrients essential to survival
Feeding behaviours may be motivated by hunger and satiety signals, but are
guided by the interaction of the senses of taste and smell
Hunger and Satiety:
Glucose and Glycogen Balance:
One of the main reasons that you feel hungry is low blood glucose levels.
Glucose is important for keeping your body's functions operating and is the
preferred source of energy for the brain; unlike other organs and tissues, the brain
cannot use fat energy stores for fuel which makes regulating glucose availability a
You are very sensitive to the level of glucose in your blood, and this directly
relates to your feelings of hunger.
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.
Some glycogen is stored in the muscles, but the main supply is in your liver where
it can be readily converted back into glucose.
This glucose-glycogen balance is mediated to a large degree by the liver and a
pancreatic hormone called insulin
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
When these levels get low enough, the liver begins to break down 'its stored
glycogen into glucose, releasing it back into circulation.
In this way, the liver and pancreas help to buffer extreme swings in blood glucose
levels. 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.
At some point, the glucose and glycogen levels get too low and you will feel
hungry. (See chart below.)
Neuropeptide Y: Another hunger cue comes from Neuropeptide Y or NPY.
High levels of NPY activity in the hypothalamus are associated with increased
appetite and food seeking behaviours - such as heading to the kitchen.
NPV affects feeding behaviour similarly in fish, reptiles, birds, and other non-
Satiety and the Liver:
What makes you stop after eating?
Just as your liver can send signals to your brain to trigger hunger it also sends
signals to the brain that trigger satiety.
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.
However, when the same glucose dose is injected into a different vein, say one
that does not directly connect to the liver; the dog will continue eating.
CCK and Meal Duration:
The small intestine also has a role to play in feelings of satiety.
food moves from your stomach to your gut, the small intestine produces
Cholecystokinin, or CCK, a hormone that is responsible for feelings of satiety or
fullness after a meal.
Receptors in the brain detect CCK, which serve as a signal to stop eating.
How do we know this? Well, scientists have found that if you inject individuals
with CCK, they report feeling satiated sooner.
In another study researchers administered CCK to rats leading to shorter than
average meal durations, compared to controls.
Interestingly, these rats who received CCK ate more total meals per day than the
controls, and the total daily intake was the same for both groups.
This shows that CCK is a short-term satiety signal.
Long-Term Weight Regulation:
Whenever possible, long-term energy storage takes place in the form of fat (i.e.
Both short-term and long-term mechanisms interact to regulate overall energy
balance and body-weight.
Why do animals store most of their excess energy in the form of fat? Why not
store it all as glycogen, which is a quickly transferable source of energy?
o Fat has more than twice the energy that carbohydrates, like glycogen,
have. For every 1 gram of fat, there are 9 units of kilocalories. Compare
that with carbohydrates which contain only 4 kilocalories per gram.
o And unlike glycogen, fat is found in virtually all parts of the body. If you
took a 70 kg man, he has about 1200 kcal of energy stored in the form of
glycogen. This would be enough to fuel his activities for 12-18 hours.
o However, that same man has approximately 120 000 kcal stored in fat -
that‘s enough energy to live off of for a couple of months!
o So for the long-term, fat is the better choice for storing more energy. But
the fat or adipose tissue is so much more than just a passive energy
storehouse. It is an active component of your regulatory physiology and
was fairly recently classified as an endocrine organ as well. Leptin:
Adipose tissue secretes a hormone called leptin, which is involved in long-term
energy balance and correlated with fat mass.
When leptin levels rise, they act on receptors in the hypothalamus to reduce
appetite food consumption decreases.
Leptin production is controlled by the OB Gene 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 the mice are given regular injections of leptin,
causing their eating behaviour and weight to return to normal.
OB Gene Revisited:
These studies suggest that a contributing factor for obesity in humans ‘may
involve defective OB genes or receptors.
However, this inference is not supported in clinical findings; very few obese
people have known defects in the leptin signalling system.
What happens if you give leptin to an obese animal who happens to have normal
leptin levels? In this case, giving additional leptin actually does not reliably result
in weight loss to return to normal levels.
It appears that humans and other animals are capable of becoming leptin resistant:
that is, at beyond a certain point, leptin's ability to inhibit appetite is reduced.
Consider that access to calories was a limited resource for most of human
evolutionary history;' taking in too many calories must have been a rare luxury.
It is more likely that the primary adaptive function of leptin was to serve as
indicator of low energy stores, rather than as a signal to directly reduce food
Low leptin levels would signal to increase foraging effort or minimize activity in
order to conserve energy.
Rarely would an individual have had very high levels of leptin or suffered from
the negative effects associated with excess adipose tissue.
What is the mechanism of leptin action? If you think of NPV activity in the
hypothalamus as the ON switch for appetite, leptin acts to inhibit the actions of
And so, the NPV mediated increase is appetite is prevented by leptin, leading to
decreased appetite and energy consumption.
Together leptin and NPV interact to regulate your weight to optimal levels.
Maladaptive Feeding and NPY:
Evidence in rats suggests that NPYergic neurons can specifically affect reward-
driven feeding for high calorie foods such as sucrose.
o In one series of experiments, NPY was injected directly into the brain of
rats who were satiated by previous food consumption. This revealed some
interesting results: first, there is an increase in the intake of sucrose.
o Second, rats will begin to work harder for a cue associated with sucrose
o Third, rats also increased the consumption of saccharin (similar taste to
sucrose but without calories)
o Finally, these rats will also preferentially choose a diet of carbohydrates
over protein, or fat. This line of research suggests that NPV action promotes unconditional and
conditional behaviours that specifically lead to increased carbohydrate
A rat‘s preexisting preferences, plays an important role in this NPV-induced
increase in carbohydrate preference; rats that showed a higher baseline preference
for carbohydrates showed the greatest preference for carbohydrates following the
These studies suggest an interesting implication for genetic predisposition toward
Another interesting hypothesis on overeating is related to endogenous opioids.
Endogenous opioids have morphine-like actions within the body and also
contribute to palatability and reward driven feeding.
Interestingly, blocking the opioid receptors with a drug called naloxone reduces
intake of rewarding foods such as saccharin and sucrose.
Consistent with this hypothesis, knock-in mice which have been genetically
modified to lack the opioid receptor show lower preference for saccharin than do
Some researchers have speculated that overeating in some people may be
reflective of a maladaptive opioid-mediated reward-driven feeding.
Energy balance and body weight regulation by hormones and mechanisms are
asymmetric. That is, the body defends itself against weight loss more strongly
than it does against weight gain.
This asymmetry can be understood from an evolutionary perspective, where
calories and nutrition were less certain. However, this asymmetry may have an
unintentional maladaptive expression in a modern, fast-food nation where calories
are cheap and physical exertion is minimal.
Taste Preferences and Food Selection:
Through the course of evolution, foods that are bitter or sour are associated with
flavours not commonly enjoyed, because they are often indicative of toxins or