Hunger & the Chemical Senses (Mar 18 , 2013)
Seeking out food and drink is a fundamental goal-directed behaviour because your moving
body needs regular nourishment to function optimally.
In many ways, life is dominated by the consumption of food and drink. 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 to survival.
In the present context, these evolutionarily driven behaviours may now seem out of place in
modern societies where calories come cheaply and easily.
Food doesn’t taste the same without your sense of smell! Feeding behaviour 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!!
Glucose and Glycogen Balance
When we’re fasting, one of the main reasons that you feel hungry is low blood glucose
Glucose is important for keeping the body’s functions operating and is the preferred
source of energy of the brain, unlike other organs and tissues, the brain can’t use fat
energy stores for fuel which makes regulating glucose availability a top priority.
We’re sensitive to the level of glucose in your blood, and this directly relates to the
feelings of hunger.
Glucose is the primary source of energy in the brain
To keep the brain constantly supplied with energy, the 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 the LIVER, where it can
be readily converted back into glucose when the circulating blood glucose levels are low.
The glucose-glycogen balance is mediated to a large degree by the liver and a pancreatic
hormone called Insulin. Glucose-Glycogen Cycle
I. When you had a meal, ur body is immediately supplied with an influx of sugar. It’s time
for the body to take action: The pancreas secretes insulin to promote the uptake of
glucose by cells in the body for immediate use, but also to stimulate storage of excess
glucose as glycogen.
II. Now, you can’t think about eating again. But at this time from the feast increases, the
blood glucose levels will correspondingly begin to dip. When these levels get low
enough, the liver begins to breakdown its stored glycogen into glucose, releasing it back
III. In this way, the liver and pancreas help to buffer extreme swings in blood glucose levels.
As the cycle continues and the time since the feast increases, your glycogen reserves in
the liver will decrease and a status signal is sent to the brain.
IV. At some point, the glucose and glycogen levels get too low and you will feel hungry
again. The glycogen stores are being depleted during the night. Eating a bowl of cereal
for breakfast increases the blood glucose levels for now and helps to replenish the
glycogen stores for later.
I. 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.
II. NPY affects feeding behaviour similarly in fish reptiles, birds and other non-human
Now, Why stop eating? Why not continue?
- As the liver can send signals to the brain to trigger hunger, it also sends signals to
the brain that trigger satiety.
- If, you inject glucose into a vein that connects directly to the liver in the dog while
he’s eating, he will stop. But if the same glucose does is injected into a different vein,
say one that does not directly connect to the liver, the dog will continue eating.
The liver monitors your glycogen stores and blood sugar levels. 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
The small intestine also has a role to play in feeling of Satiety.
As the bowl of cheerios move from the stomach to the 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? Studies found that if you inject individuals with CCK, they report
feeling satiated sooner. Or, researches administered CCK to rats leading to shorter than
average meal durations, compared to controls. 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.
That shows CCK is a short-term satiety signal. The main reason why we only ate 1 bowl
of cereal instead of 12.
CCK appears to regulate short-term feeding behaviours, like ending a meal, but not long-
tern 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. Both short-term and long-term mechanisms interact to
regulate overall energy balance and body-weight.
a. Why do animals store most of their excess energy in the form of fat? Why not stored it
all as glycogen, which is a quickly transferable source of energy?
b. Fat has more than twice the energy that carbohydrates, like glycogen has. For every 1g
of fat, there are 9 units of kilocalories. For 1g of carbohydrates, there are only 4kcal.
c. Also, unlike glycogen, fat is found in virtually all parts of the body. If you took a 70ky
man, ha has about 1200 kcal of energy stored in the form of glycogen. This could fuel his
activities for 12-18 hours.
d. But if he has approximately 1200 kcal stored in fat, it could last him a couple of months!
So fat is the better choice for storing more energy.
e. 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.
f. Leptin: a hormone secretes by the adipose tissue; 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 and, consequently, food consumption decreases.
g. Leptin production is controlled by the OB gene. OB Gene regulates leptin production.
h. In genetically altered knock-out mice lacking an OB Gene, 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.
i. 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.
j. What happens if you give leptin to an obese animal who happens to have normal leptin
levels? In this case, giving additional leptin actually doesn’t reliably result in weight loss
to return to normal levels. It appears that humans and other animals are capable of
becoming leptin resistant: at beyond a certain point, leptin’s ability to inhibit appetite is
k. The 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 intake.
l. 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.
m. What is the mechanism of leptin action? If NPY activity in the hypothalamus acts as the
ON switch for appetite, leptin acts to inhibit the actions of NPY. And so, the NPY
mediated increase is appetite is prevented by leptin, leading to decreased appetite and
energy consumption. Together, leptin and NPY interact to regulate your weight to
Maladaptive Feeding & Neuropeptide Y
I. NPY increased intake of sucrose, and intake of saccharin.
II. In one series of expts, NPY was injected directly into the brain of rats who were satiated
by previous food consumption.
III. There si an increase in the intake of sucrose.
IV. Rats will begin to work harder for a cue associated with sucrose.
V. Rats also increased the consumption of saccharin (similar taste to sucrose but without
VI. These rats will also preferentially choose a diet of carbohydrates over protein, or fat.
VII. This line of research suggests that NPY action promotes unconditional and conditional
behaviour that specifically lead to increased carbohydrate consumption.
VIII. A rat’s pre-existing preferences plays an important role in this NPY-induced increase in
carbohydrate preference. Rats that showed a higher baseline preference for
carbohydrates showed the greatest preference for carbohydrates following the NPY
I. Naturally occurring chemical substances that have morphine-like analgesic actions in the
body II. Contributes to palatability and reward-driven feeding
III. Blocking the opioid receptors with a drug called naloxone causes Naloxone reduces
intake of saccharin, sucrose and saline
IV. Consistent with this hypotheses, knock-in mice which have been genetically modified to
lack the opioid receptor show lower preference for saccharin than do control mice.
Some researchers have speculated that ov