3. Physiological Regulatory Mechanisms
A regulatory mechanism contains four essential features:
• the system variable (the characteristic
• to be regulated), a set point (the optimal value of the system
variable),
• a detector that monitors the value of the system variable,
• and a correctional mechanism that restores the system variable to
the set point.
• The activity of the system is regulated by negative feedback, a
process whereby the effect produced by an action serves to diminish
or terminate the action.
4. An example of a regulatory system is a room
whose temperature is regulated by a
thermostatically controlled heater. The system
variable is the air temperature of the room, and
the detector for this variable is a thermostat.
This device can be adjusted so that contacts of
a switch will be closed when the temperature
falls below a preset value (the set point).
Closure of the contacts turns on the
correctional mechanism—the coils of the
heater. If the room cools below the set point of
the thermostat, the thermostat turns the heater
on, and the heater warms the room. The rise in
room temperature causes the thermostat to
turn the heater off. Because the activity of the
correctional mechanism (heat production) feeds
back to the thermostat and causes it to turn the
heater off, this process is called negative
feedback. Negative feedback is an essential
characteristic of all regulatory systems.
5. Ingestive Behaviors : Drinking
• Ingestive behaviors are correctional mechanisms that replenish the body’s depleted stores of water or
nutrients. Because of the delay between ingestion and replenishment of the depleted stores, ingestive
behaviors are controlled by satiety mechanisms as well as by detectors that monitor the system
variables.
• Satiety mechanisms are brain-based mechanisms that reduce hunger or thirst related to behaviors that
result in adequate intake of nutrients or water. Satiety mechanisms are required because of the
physiology of our digestive system. For example, suppose you spend some time in a hot, dry
environment and lose body water.
• The loss of water causes internal detectors to initiate the correctional mechanism: drinking. You quickly
drink a glass or two of water and then stop. What stops your ingestive behavior? The water is still in your
digestive system, and has not yet moved into the fluid surrounding your cells, where it is needed.
Therefore, although drinking was initiated by detectors that measure your body’s need for water, it was
stopped by other means.
• There must be a satiety mechanism that says, in effect, “Stop—this water, when absorbed by the
digestive system into the blood, will eventually replenish the body’s need.” Satiety mechanisms monitor
the activity of the correctional mechanism (in this case, drinking), not the system variables themselves.
When a sufficient amount of drinking occurs, the satiety mechanisms stop further drinking in anticipation
of the replenishment that will occur later.
6.
7. Types of Thirst – Fluids involved
• Intracellular fluid The fluid
contained within cells.
• Extracellular fluid All body fluids
outside cells: interstitial fluid,
blood plasma, and cerebrospinal
fluid.
• Intravascular fluid The fluid
found within the blood vessels.
• Interstitial fluid The fluid that
bathes the cells, filling the space
between the cells of the body (the
“interstices”).
8. Cont..
• Approximately two-thirds of the body’s water is contained in the intracellular fluid, the
fluid portion of the cytoplasm of cells. The rest is extracellular fluid, which includes
intravascular fluid (the blood plasma), cerebrospinal fluid, and interstitial fluid (fluid
that bathes our cells).
• The volume of intracellular and intravascular fluid must be kept within precise limits.
Losing intracellular water deprives cells of the ability to perform many chemical reactions,
and gaining water can cause their membranes to rupture.
• The volume of intravascular fluid must be closely regulated because of the mechanics of
the operation of the heart. If the blood volume falls too low, the heart can no longer pump
the blood effectively; if the volume is not restored, heart failure will result. This condition is
called hypovolemia.
• Intracellular and intravascular fluids are monitored by two different sets of receptors: one
measuring cell volume (intracellular) and another measuring blood volume (intravascular).
9. Most of the time, we ingest more water than we need, and the kidneys excrete the excess.
However, if the levels of water fall too low, correctional mechanisms— drinking water—are
activated.
Because loss of water from either the intracellular or intravascular fluid compartments stimulates
drinking, researchers have adopted the terms osmometric thirst and volumetric thirst to describe
them.
Osmometric thirst occurs when the solute concentration of the interstitial fluid increases.
Solutes are substances, such as salts, dissolved in a solution. An increase in interstitial solute
concentration draws water out of the cells, and they shrink in volume.
Osmoreceptors are neurons whose firing rate is affected by their level of hydration. That is, if the
interstitial fluid surrounding them becomes more concentrated, they lose water through osmosis.
The shrinkage causes them to alter their firing rate, which sends signals to other parts of the
brain.
10.
11. The osmoreceptors responsible for osmometric thirst are located in the lamina terminalis. The
lamina terminalis contains two specialized circumventricular organs: the OVLT and the SFO. These
structures are found in the hypothalamus, in a region that borders the anteroventral tip of the third
ventricle (the AV3V). These brain regions lack a blood–brain barrier (McKinley and Johnson, 2004).
Injections of concentrated saline directly into this region produce drinking (Buggy, 1979).
Intravenous injections of concentrated saline into human volunteers activates several brain regions,
including the AV3V and the anterior cingulate cortex (Egan et al., 2003).
When the volunteers were permitted to drink water, they did so, and almost immediately reported
that their thirst had been satisfied. Simultaneously, the activity in the anterior cingulate cortex
returned to baseline values. However, the activity in the AV3V remained high.
These results suggest that the activity of the anterior cingulate cortex reflected the volunteers’ thirst,
which was immediately relieved by a drink of water.
In contrast, the continued activity in the AV3V reflected the fact that the blood plasma still contained
increased salt concentrations. It takes around 20 minutes for a drink of water to be absorbed into
the general circulation.
12. Volumetric thirst
• Volumetric thirst occurs when the volume of the blood plasma—the
intravascular volume—decreases. When we lose water through
evaporation, we lose it from all three fluid compartments: intracellular,
interstitial, and intravascular.
• This means that evaporation produces both volumetric thirst and
osmometric thirst. In addition, loss of blood, vomiting, and diarrhea all
cause loss of blood volume (hypovolemia) without depleting the
intracellular fluid.
• Blood loss is the most obvious cause of pure volumetric thirst. From the
earliest recorded history, reports of battles note that the wounded survivors
called out for water. In addition, because hypovolemia involves a loss of
sodium as well as water, volumetric thirst leads to a salt appetite.
13. • Detector cells in the heart and kidneys help monitor blood volume and
induce volumetric thirst when intravascular fluid is low. Cells in the kidneys
detect decreases in blood flow. In response to low blood volume, the
kidneys are responsible for the presence of the hormone angiotensin
following a cascade of biochemical events.
• Angiotensin initiates drinking and a salt appetite, causes the kidneys to
conserve water and salt, and increases blood pressure. Therefore,
reduced blood flow to the kidneys causes water and salt to be retained,
encourages the animal to find and ingest water and salt, and allows the
organism to compensate for reduced blood volume until fluid balance can
be restored.
• A second set of receptors for volumetric thirst is located in the atria of the
heart. These baroreceptor cells are stretch sensitive and detect when
blood volume in the heart falls. Reduced blood flow to the heart increases
drinking and severing the nerves to the atrial baroreceptors decreases
drinking, demonstrating the important role of these receptor cells
(Fitzsimmons and Moore-Gillon, 1980; Quillen et al., 1990).
14. Eating
• Eating is one of the most important things we do, and it can also be one of the
most pleasurable. The control of eating is even more complicated than the control
of drinking.
• We can achieve water balance by the intake of two ingredients: water and salt.
When we eat, we must obtain adequate amounts of carbohydrates, fats, amino
acids, vitamins, and minerals other than sodium.
• To stay alive, our cells must have fuel and oxygen. Fuel comes from the digestive
tract, and its presence there is a result of eating. But the digestive tract is
sometimes empty; in fact, most of us wake up in the morning in that condition.
• So there has to be a reservoir that stores nutrients to keep the cells of the body
nourished when the gut is empty. There are two reservoirs: one short-term and
the other long-term. The short-term reservoir stores carbohydrates, and the long-
term reservoir stores fats.
15. The Short-Term Reservoir
• The short-term reservoir sustains our fuel needs for several hours between meals. It is located in
the cells of the liver and the muscles, and it is filled with a complex, insoluble carbohydrate called
glycogen. Cells in the liver convert glucose (a simple, soluble carbohydrate) into glycogen and
store the glycogen. They are stimulated to do so by the presence of insulin, a peptide hormone
produced by the pancreas.
• When glucose and insulin are present in the blood, some of the glucose is used as a fuel, and some
of it is stored as glycogen.
• Later, when all of the food has been absorbed from the digestive tract, the level of glucose in the
blood begins to fall. The fall in glucose is detected by cells in the pancreas and in the brain. The
pancreas responds by stopping its secretion of insulin and starting to secrete a different peptide
hormone: glucagon.
• The effect of glucagon is opposite that of insulin: It stimulates the conversion of glycogen (stored in
the liver) into glucose. The liver stores excess glucose as glycogen when plenty of glucose is
available, and it releases glucose from its reservoir when the digestive tract empties and the level of
glucose in the blood begins to fall.
16.
17. The carbohydrate reservoir in the liver is reserved primarily for the central
nervous system (CNS).
When you wake in the morning, your brain is being fed by your liver, which is in
the process of converting glycogen to glucose and releasing it into the blood. The
glucose reaches the CNS, where it is absorbed and metabolized by the neurons
and the glia.
This process can continue for a few hours, until all of the carbohydrate reservoir
in the liver is used up.
Usually, we eat some food before this reservoir gets depleted, which permits us
to refill it. But if we do not eat, the CNS (and the rest of the body) must start living
on the products of the long-term reservoir.
18. The Long Term Reservoir
Our long-term reservoir consists of adipose tissue (fat tissue). This reservoir is filled with triglycerides.
Triglycerides are complex molecules that contain glycerol (a soluble carbohydrate, also called glycerine)
combined with three fatty acids (stearic acid, oleic acid, and palmitic acid). Adipose tissue is found beneath the
skin and in various locations in the abdominal cavity. It consists of cells that are capable of absorbing nutrients
from the blood, converting them to triglycerides, and storing them.
These cells can expand in size. For example, the primary physical difference between a person who is obese
and a person who is not is the size (and not the number) of their fat cells. The size of the fat cells is determined
by the amount of triglycerides the cells contain.
The long-term fat reservoir is what keeps us alive when we are fasting. As we begin to use the contents of our
short-term carbohydrate reservoir, fat cells start converting triglycerides into fuels that the cells can use and
releasing these fuels into the bloodstream.
When we wake in the morning with an empty digestive tract, our brain (in fact, all of the CNS) is living on glucose
released by the liver. The other cells of the body are living on fatty acids, reserving the glucose for the brain.
19. When the digestive system is empty, activity of the sympathetic axons
that innervate adipose tissue, the pancreas, and the adrenal medulla,
increases. All three effects (direct neural stimulation, secretion of
glucagon, and secretion of catecholamines) cause triglycerides in the
long-term fat reservoir to be broken down into glycerol and fatty acids.
The fatty acids can be directly metabolized by cells in all of the body
except the brain, which needs glucose.
That leaves glycerol. The liver takes up glycerol and converts it to
glucose. That glucose, too, is available to the brain.
20. Obesity – (Robles , Kuo & Galván, 2021)
Neuroscience is a field that elucidates the underlying mechanisms that motivate individuals to eat, which in
excess, may result in overweight and obesity.
The prefrontal cortex or “control” region of the brain, in addition to other functions, helps individuals control
their behavior, inhibit their impulsive responses, and evaluate and make decisions about environmental stimuli.
Several studies have found that overeating (i.e., a behavior linked to overweight/obesity) is attributed to
impaired inhibitory control in networks of the brain where the prefrontal cortex is a key node.
The limbic system, a set of brain structures connected to the prefrontal cortex, also shapes individuals'
motivation behaviors. For example, there is evidence that the mesolimbic structures of the brain, and the
“reward pathway” of the brain, are responsible for the hedonic aspects of eating and incentive salience in food
motivation behaviors.
Adult binge eaters appear to have a lower activation in the fronto-striatal (limbic) region of the brain, and
greater trait impulsivity and lower inhibitory control abilities, compared to non-binge eaters. It also appears
that adolescents with food addiction experience this condition due to hypo-activation in areas of the brain that
inhibit control.
21.
22. Eating Disorders – Anorexia
Anorexia is associated with loss of gray and
white matter in the brain (Seitz et al., 2016).
Some reports (Artmann et al., 1985;
Golden et al., 1996; Herholz, 1996;
Katzman et al., 2001; Kingston et al., 1996)
indicate the presence of enlarged ventricles
and widened sulci in the brains of patients
with anorexia, which indicate shrinkage of
brain tissue.
However, not all brain areas seem to be
equally affected by volume reduction.
Specifically, the frontoparietal – cingulate
network involved in perception and
integration of body stimuli seems to be
reduced in volume.
Some research suggests that this tissue
loss can be reversed with successful
treatment of the eating disorder (Golden et
al., 1996; Seitz et al., 2016)
23.
24. Excessive Exercise
Excessive exercising is a prominent symptom of anorexia (Zandian et al., 2007). Studies with animals suggest that the
increased physical activity may be a result of fasting or food restriction. When rats are allowed access to food for one hour
each day, they will spend more and more time running in a wheel if one is available and will lose weight and eventually die
(Smith, 1989). One explanation for the increased activity of rats on a semistarvation diet is that it reflects an innate tendency to
seek food when it becomes scarce. Normally, hungry rats would extend their activity by exploring the environment and
searching for food, but because of their confinement the tendency to explore is expressed through wheel running. The fact that
starving rats increase their activity suggests that the excessive activity of patients with anorexia may be a symptom of
starvation,
not a weight-loss strategy.
Blood levels of NPY (Neuropeptide Y) are elevated in patients with anorexia. Nergårdh et al. (2007) found that infusion of NPY
into the cerebral ventricles further increased the time spent running in rats on a restricted feeding schedule. Normally, NPY
stimulates eating (as it does in rats with unlimited access to food), but under conditions of starvation it stimulates wheel-running
activity instead. The likely explanation for this phenomenon is that, if food is not present, NPY increases the animals’ activity
level, which would normally increase the likelihood that they would find food. Increased levels of NPY may also play a role in
the obsession with food that is often seen in patients with anorexia.
Functions of NPY include: increasing food intake and storage of energy as fat, reducing anxiety and stress, reducing pain perception, affecting the
circadian rhythm, reducing voluntary alcohol intake, lowering blood pressure, and controlling epileptic seizures.
