CHAPTER 10
INTERNAL REGULATION
Chapter Outline
I.
Temperature Regulation
1. Several species of animals have developed behaviors designed to regulate
body temperature.
a. A small male garter snake produces female pheromones and attract larger
males, who, in the process of trying to copulate with the smaller male,
warm him.
b. Some bird species that stand on one leg do so in cold weather so that the
other leg is warmed under their body.
c. Vultures sometimes defecate on their legs on hot days so that the
evaporation process cools them.
d. Toucans have huge bills so that they can direct blood flow to the bill and
either cool or warm themselves accordingly.
e. Lizards huddle to protect themselves against rapidly changing
temperatures.
2. Homeostasis and Allostasis
a. Homeostasis: Temperature regulation and other biological processes that
keep certain body variables within a fixed range.
b. Set point: Level at which a homeostatic process maintains a variable.
c. Negative feedback: Processes that reduce discrepancies from the set
point.
d. Allostasis: Dynamic and adaptive changes in the body’s set points in
response to changes in its life or changes in the environment.
3. Controlling Body Temperature
a. Temperature regulation is a high biological priority.
b. Basal Metabolism: Energy used to maintain a constant body temperature
at rest. Twice as much energy is used for temperature regulation as all
other activities combined.
c. Poikilothermic: Animals with body temperatures the same as their
environment (i.e., fish and lizards).
d. Homeothermic: Animals with physiological mechanisms that maintain an
almost constant body temperature despite variations in environmental
temperature. These types of animals generate heat in proportion to their
total mass but radiate heat in proportion to their surface area. For these
animals, sweating, licking themselves, and panting are used as cooling
mechanisms. Shivering and fluffing are used as heating mechanisms.
d. The Advantages of Constant High Body Temperature
•
Mammals maintain a body temperature of 37C because maintaining a
high body temperature keeps the animal ready for rapid movement
even in cold temperatures.
• Mammals may have developed even higher body temperatures except
that proteins become unstable at temperatures above 40C.
• Reproductive cells require a somewhat cooler temperature than other
body cells.
e. Brain Mechanisms
• The brain regions most critical for temperature control are the anterior
hypothalamus and the preoptic area of the hypothalamus (preoptic
because it is near the optic chiasm). Because of the close relationship
between these areas, they are often treated as one area, the preoptic
area/anterior hypothalamus (POA/AH).
• The POA/AH monitors body temperature by monitoring its own
temperature and by receiving input from temperature-sensitive skin
and spinal cord receptors.
e. Fever
• Infection of the body by bacteria or viruses causes fever. The fever is
not a part of the illness; it is instead a part of the body’s defenses.
Once infected, the body mobilizes its leukocytes (white blood cells) to
attack these foreign substances. Leukocytes release small proteins
called cytokines, which attack the intruders and communicate with the
brain.
• A fever represents an increased set point for body temperature.
Moving to a cooler room will not lower a fever; it will just cause the
body to work harder to maintain its temperature.
• Newborn rabbits, whose hypothalamus is immature, prefer a room
warm enough to increase their body temperature in response to an
infection. In other words, they develop a fever by behavioral means.
• Fever works because certain types of bacteria grow less vigorously at
high temperatures, and it enhances the activity of the immune system.
However, a fever above 39C does more harm than good, and a fever
above 41C is life threatening.
II. Thirst
A. Mechanisms of Water Regulation
B. Different species have different strategies for maintaining water. Humans, like
beavers, drink more than is needed and excrete the rest.
C. For humans, when your body needs water, the posterior pituitary gland releases
vasopressin, also known as antidiuretic hormone (ADH), which enables the
kidneys to reabsorb water and secrete highly concentrated urine.
D. Osmotic Thirst
1. Thirst can be divided into two types: thirst due to eating salty foods
(osmotic thirst) and thirst due to a loss of fluids (hypovolemic thirst).
2.
3.
Osmotic pressure: The tendency of water to flow across a semipermeable
membrane from an area of low concentration to areas of high concentration.
In cells, the membrane works as a semipermeable membrane and water, but
not all solutes, flows freely between the extracellular fluid (fluid outside the
cell) and intracellular fluid (fluid inside the cell).
Osmotic thirst: Occurs when certain neurons detect their own loss of
water. This loss of water happens when solute concentrations in the
extracellular fluid are higher than the concentration of solutes in the
intracellular fluid, causing water to be drawn from the intracellular
compartment to dilute the solutes in the extracellular fluid.
4. Organum Vasculosum Laminae Terminalis (OVLT) and subfornical
organ: Areas located around the third ventricle that are responsible for
detecting osmotic pressure.
5. The brain also receives information from receptors in the periphery,
including the stomach, that detect high levels of sodium.
6. The supraoptic nucleus and paraventricular nucleus are brain areas
located in the hypothalamus that control the rate at which the posterior
pituitary gland releases vasopressin. Both of these brain areas and the
lateral preoptic area (which controls drinking) receive information from
the OVLT, the subfornical organ, the stomach, and elsewhere.
7. Mechanisms exist that prevent too much water consumption. The body
monitors swallowing and detects the water contents of the stomach and
intestines. Those messages suppress thirst long before the ingested water
can reach the brain.
C. Hypovolemic Thirst and Sodium-Specific Hunger
1. When you lose a significant amount of body fluid by bleeding, diarrhea, or
sweating, the body will release hormones, including vasopressin and
angiotensin II, that constrict blood vessels. When blood volume decreases,
kidneys release the hormone rennin, which splits a portion off
angiotensinogen (a large protein in the blood) to form angiotensin I, which
is then converted into angiotensin II; this hormone constricts blood vessels
in order to reverse the loss of blood volume.
2. Angiotensin II triggers hypovolemic thirst (thirst based on low volume).
During hypovolemic thirst the body needs to replenish both water and lost
solutes such as salt.
3. Whereas an animal with osmotic thirst needs water, one with hypovolemic
thirst can’t drink much pure water because it would dilute its body fluids.
4. Specific sodium cravings (due to bleeding or excessive sweating) are
caused by the release of aldosterone, a hormone which causes the kidneys,
salivary glands, and sweat glands to conserve sodium and excrete more
watery fluids than usual. Aldosterone and angiotensin II together change the
properties of the neurons in the nucleus of the tractus solitarius (part of the
taste system) such that they begin reacting to salt in nearly the same way
they would to sugar.
III. Hunger
A. Digestion and Food Selection
1. Digestion begins in the mouth, where food is broken down by enzymes in
the saliva. Food then travels down the esophagus to the stomach, where
hydrochloric acid and enzymes digest proteins. A round sphincter muscle
(located between the stomach and the intestines) allows food to periodically
enter the intestines. Food then enters the small intestine, which is the main
site for nutrient absorption into the bloodstream.
These digested nutrients are carried by the blood to cells throughout the
body, which use some of the nutrients and store the rest as excess. The large
intestine absorbs water and minerals and lubricates remaining materials for
excretion.
2. Consumption of Dairy Products
a. Newborn mammals survive on mother’s milk and then eventually stop
nursing.
b. Many mammals lose the intestinal enzyme lactase, which allows them
to metabolize lactose (sugar found in milk). Losing the enzyme lactase
may be an evolved mechanism to encourage weaning.
c. Milk consumption then causes stomach cramps and gas.
d. The ability to consume large amounts of milk products varies
geographically. In China and surrounding countries, nearly everyone
lacks the ability to metabolize lactose.
3. Food Selection and Behavior
a. Many unsubstantiated myths exist about food selection and behavior,
including the idea that turkey makes you sleepy because of its
tryptophan content and sugar makes kids hyperactive.
b. The belief that fish is brain food has support. Recent studies suggest
that fish contain oils that are helpful for brain functioning, including
memory and reasoning abilities.
B. Short- and Long-term Regulation of Feeding
1. The brain gets messages from the mouth, stomach, intestines, fat cells, and
elsewhere to regulate eating.
2. Oral Factors
a. Tasting and chewing food is an important part of eating. Participants in
a study where liquid food was pumped in their stomachs found the
meals unsatisfying and reported a desire to taste or chew something.
b. In sham-feeding experiments, everything an animal eats leaks out a
tube connected to the esophagus or stomach (under these conditions,
animals consume several times as much as untreated animals during
each meal).
c. These studies demonstrate that although taste and mouth are important
cues, they are not sufficient alone to produce satiety.
3. Stomach and Intestines
a.
3.
4.
Usually, we end a meal before the food reaches the blood. Satiety
signals are therefore based on other aspects of eating such as stomach
distension.
b. Studies show that stomach distention is sufficient to produce satiety,
though not necessary because those with stomachs surgically removed
still report satiety.
c. The vagus nerve (cranial nerve X) carries information to the brain
regarding the stretching of stomach walls, providing a major basis for
satiety.
d. The splanchnic nerves convey information about the nutrient contents
of the stomach, carrying impulses back and forth from the spinal cord
to the digestive organs.
e. The duodenum is part of the small intestine adjoining the stomach.
The duodenum also releases a hormone called oleoylethanolamide
(OEA) to cause satiety.
f. Cholecystokinin (CCK): A hormone released by the duodenum to
inhibit appetite.
Glucose, Insulin, and Glucagon
a. Insulin: Facilitates entry of glucose from the bloodstream into the
body's cells. (Brain cells do not need insulin for glucose to enter).
b. Glucagon: Stimulates the liver to convert stored glycogen to glucose.
c. After a meal, insulin levels rise, glucose readily enters the cell, and
appetite decreases. As time passes, blood glucose levels fall, the body
causes an increase in glucagon release, and hunger is induced.
d. Chronically high insulin levels causes increased eating because blood
glucose levels are low. In autumn, animals getting ready for
hibernation experience rapid weight gain because of high insulin levels.
Humans also eat more in autumn that in other seasons.
e. Diabetics eat more food than usual but excrete much of their glucose
and lose weight due to poor insulin blood levels.
Leptin
a. A recently discovered hormone that monitors the body’s fat reserves to
account for day-to-day mistakes in consumption.
b. Leptin is normally made by fat cells so that the more fat cells, the
higher the levels of leptin. When fat cell reserves are low, there are low
levels of leptin and hunger increases.
c. Each meal also releases leptin, as a short-term monitor about the body;s
fat reserves.
d. Some mice genetically predisposed to obesity fail to produce leptin.
The brain then acts as if the body has no fat stores and signals the
mouse to eat more and be less active (to conserve energy). Leptin
injections have reversed these symptoms in mice.
e. Humans become less sensitive to leptin during pregnancy. Obesity also
lowers leptin sensitivity by damaging the endoplasmic reticulum in
neurons of the hypothalamus. This can only be reversed through
physical exercise.
C. Brain Mechanisms
1. The Arcuate Nucleus and Paraventricular Hypothalamus
a. The arcuate nucleus of the hypothalamus has a set of neurons sensitive
to hunger signals and another set of cells sensitive to satiety signals.
The hunger-sensitive cells receive input from the taste pathway and
from ghrelin (a neurotransmitter released from the stomach during
periods of food deprivation), released by axons.
b. The satiety-sensitive cells receive input for both short-and long-term
satiety. Input includes CCK release from the intestines, and insulin
release from both blood glucose and body fat. Leptin also provides
input to the arcuate nucleus.
c. Much of the input from the arcuate nucleus goes to the
paraventricular nucleus (PVN). The PVN inhibits the lateral
hypothalamus (an area important for eating) and is involved in satiety.
If the PVN is damaged, rats eat larger than normal meals.
d. α-Melanocyte stimulating hormone is released from the satietysensitive cells of the arcuate nucleus to the PVN. Deficiencies in
melanocortin receptors cause people to overeat as they do not respond
to satiety signals.
e. Inhibitory transmitters from the hunger-sensitive cells of the arcuate
nucleus including GABA, neuropeptide Y (NPY), and agouti-related
peptide (AgRP) inhibit the PVN and the satiety-sensitive cells of the
arcuate nucleus.
f.NPY cells also have a pathway to the orexin-producing cells of the lateral
hypothalamus. Orexin stimulates activity and the onset of meals but has
a minor overall effect on feeding behavior.
2. The Lateral Hypothalamus
a. The lateral hypothalamus controls insulin secretion, alters taste
responsiveness, and facilitates feeding in other ways. Damage to the
lateral hypothalamus causes an animal to refuse food and water.
b. Contributions of the lateral hypothalamus include: altering the taste of
food (when one is hungry, food tastes better), causing cortical cells to
increase their response to taste, smell, or sight of food, controlling
insulin secretion, controlling digestive secretions.
3. Medial Areas of the hypothalamus
a. Ventromedial hypothalamus (VHM): Damage centered around this
area leads to overeating and weight gain (after gaining weight, these
animals become picky eaters, as they consume bitter foods far less than
normal but eat more than normal of a sweetened or normal diet).
However, this effect, known as the ventromedial hypothalamic
syndrome, usually requires the lesion to extend outside the
ventromedial nucleus and invade nearby axons.
D. Eating Disorders
1. Obesity and anorexia exist on different sides of the spectrum of eating
disorders.
2.
3.
4.
5.
2.
6.
Research shows that when given the option of a “buffet” of high-calorie
foods, rats are unable to pass up the options. Soon they become obese and
lose interest in rewards other than food. Humans show the same tendency.
Recent research shows that there is little correlation between obesity and
mood. This goes against the notion that obesity is caused by psychological
issues such as depression.
Exposure to a high-fat diet before birth predisposes the offspring to
increased appetite and body weight.
Genetics and Body Weight
a. A Danish study showed that the weights of adopted children correlated
better with their biological parent than their adopted family. This could
be evidence for either a genetic or prenatal environmental contribution
to weight.
b. Specific genes have been linked with obesity. A mutated gene for
melanocortin can cause obesity.
c. Syndromal obesity: obesity that results from a medical condition. The
genetic disorder Prader-Willi syndrome leads to obesity, possibly by
inducing high levels of the peptide ghrelin.
d. Most cases of obesity result from the combined influences of genes and
the environment.
Weight Loss
a. Obesity is now classified as a disease in the United States.
b. Dieting alone is rarely effective when done alone. This is because most
obese people will fail to sustain the diet. Psychologists now suggest
implementing small changes.
c. Changing lifestyle including increasing exercise and decreasing eating
is most effective. This combination helped 20-40% of people keep
weight off for at least two years.
d. Non-diet soft drinks contain fructose, a sugar that does not stimulate
normal satiety pathways. Diet soft drinks contain artificial sugars that
cause the body to unlearn the association between the taste of “sweet”
and calories.
e. Appetite suppressants such as sibutramine (Meridia), and drugs that
block fat absorption such as orlistat (Xenical) can be effective.
f. Gastric bypass surgery removes part of the stomach so that smaller
meals produce satiety.
Bulimia Nervosa
a. Condition in which people alternate between dieting and overeating.
b. Some individuals with this disorder force vomiting after meals.
c. Most bulimics suffer from depression, anxiety, or other emotional
problems.
d. People with bulimia have lower than normal levels of CCK, increased
release of ghrelin, and alterations in several other hormones and
transmitters that regulate eating. These changes are likely a product to
e.
bulimia and not the cause. After therapy, the ghrelin and other body
chemicals return toward normal levels.
Bulimia shares many similarities with drug addiction. Eating tasty
foods activate the same brain areas as addictive drugs, such as the
nucleus accumbens.