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prepared by Vince Austin,
Bluegrass Technical
and Community College
CHAPTER
Elaine N. Marieb
Katja Hoehn
24
PART B
Human
Anatomy
& Physiology
SEVENTH EDITION
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Nutrition,
Metabolism,
and Body
Temperature
Regulation
Oxidation of Amino Acids

Transamination – switching of an amine group
from an amino acid to a keto acid (usually ketoglutaric acid of the Krebs cycle)

Typically, glutamic acid is formed in this process
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Oxidation of Amino Acids


Oxidative deamination – the amine group of
glutamic acid is:

Released as ammonia

Combined with carbon dioxide in the liver

Excreted as urea by the kidneys
Keto acid modification – keto acids from
transamination are altered to produce metabolites
that can enter the Krebs cycle
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Synthesis of Proteins

Amino acids are the most important anabolic
nutrients, and they form:

All protein structures

The bulk of the body’s functional molecules
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Synthesis of Proteins


Amounts and types of proteins:

Are hormonally controlled

Reflect each life cycle stage
A complete set of amino acids is necessary for
protein synthesis

All essential amino acids must be provided in the
diet
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Summary: Carbohydrate Metabolic Reactions
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Table 24.4.1
Summary: Lipid and Protein Metabolic
Reactions
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Table 24.4.2
State of the Body

The body exists in a dynamic catabolic-anabolic
state

Organic molecules (except DNA) are continuously
broken down and rebuilt

The body’s total supply of nutrients constitutes its
nutrient pool
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State of the Body

Amino acid pool – body’s total supply of free
amino acids is the source for:

Resynthesizing body proteins

Forming amino acid derivatives

Gluconeogenesis
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Carbohydrate/Fat and Amino Acid Pools
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Figure 24.16
Interconversion Pathways of Nutrients

Carbohydrates are easily and frequently converted
into fats

Their pools are linked by key intermediates

They differ from the amino acid pool in that:

Fats and carbohydrates are oxidized directly to
produce energy

Excess carbohydrate and fat can be stored
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Interconversion Pathways of Nutrients
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Figure 24.17
Absoprtive and Postabsorptive States

Metabolic controls equalize blood concentrations
of nutrients between two states

Absorptive


The time during and shortly after nutrient intake
Postabsorptive

The time when the GI tract is empty

Energy sources are supplied by the breakdown of
body reserves
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Absoprtive State

The major metabolic thrust is anabolism and
energy storage

Amino acids become proteins

Glycerol and fatty acids are converted to
triglycerides

Glucose is stored as glycogen

Dietary glucose is the major energy fuel

Excess amino acids are deaminated and used for
energy or stored as fat in the liver
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Absoprtive State
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Figure 24.18a
Principal Pathways of the Absorptive State


In muscle:

Amino acids become protein

Glucose is converted to glycogen
In the liver:

Amino acids become protein or are deaminated to
keto acids

Glucose is stored as glycogen or converted to fat
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Principal Pathways of the Absorptive State

In adipose tissue:


Glucose and fats are converted and stored as fat
All tissues use glucose to synthesize ATP
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Principal Pathways of the Absorptive State
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Figure 24.18b
Insulin Effects on Metabolism

Insulin controls the absorptive state and its
secretion is stimulated by:

Increased blood glucose

Elevated amino acid levels in the blood

Gastrin, CCK, and secretin
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Insulin Effects on Metabolism

Insulin enhances:

Active transport of amino acids into tissue cells

Facilitated diffusion of glucose into tissue
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Insulin Effects on Metabolism
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Figure 24.19
Diabetes Mellitus

A consequence of inadequate insulin production or
abnormal insulin receptors

Glucose becomes unavailable to most body cells

Metabolic acidosis, protein wasting, and weight
loss result as fats and tissue proteins are used for
energy
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Postabsorptive State

The major metabolic thrust is catabolism and
replacement of fuels in the blood

Proteins are broken down to amino acids

Triglycerides are turned into glycerol and fatty
acids

Glycogen becomes glucose

Glucose is provided by glycogenolysis and
gluconeogenesis

Fatty acids and ketones are the major energy fuels

Amino acids are converted to glucose in the liver
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Postabsorptive State
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Figure 24.20a
Principle Pathways in the Postabsorptive
State
 In muscle:

Protein is broken down to amino acids

Glycogen is converted to ATP and pyruvic acid
(lactic acid in anaerobic states)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Principle Pathways in the Postabsorptive
State
 In the liver:

Amino acids, pyruvic acid, stored glycogen, and fat
are converted into glucose

Fat is converted into keto acids that are used to
make ATP

Fatty acids (from adipose tissue) and ketone bodies
(from the liver) are used in most tissue to make
ATP

Glucose from the liver is used by the nervous
system to generate ATP
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Principle Pathways in the Postabsorptive
State
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Figure 24.20b
Hormonal and Neural Controls of the
Postabsorptive State

Decreased plasma glucose concentration and rising
amino acid levels stimulate alpha cells of the
pancreas to secrete glucagon (the antagonist of
insulin)

Glucagon stimulates:

Glycogenolysis and gluconeogenesis

Fat breakdown in adipose tissue

Glucose sparing
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Influence of Glucagon
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Figure 24.21
Hormonal and Neural Controls of the
Postabsorptive State

In response to low plasma glucose, the sympathetic
nervous system releases epinephrine, which acts on
the liver, skeletal muscle, and adipose tissue to
mobilize fat and promote glycogenolysis
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Liver Metabolism

Hepatocytes carry out over 500 intricate metabolic
functions
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Liver Metabolism

A brief summary of liver functions

Packages fatty acids to be stored and transported

Synthesizes plasma proteins

Forms nonessential amino acids

Converts ammonia from deamination to urea

Stores glucose as glycogen, and regulates blood
glucose homeostasis

Stores vitamins, conserves iron, degrades
hormones, and detoxifies substances
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Cholesterol

Is the structural basis of bile salts, steroid
hormones, and vitamin D

Makes up part of the hedgehog molecule that
directs embryonic development

Is transported to and from tissues via lipoproteins
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Cholesterol

Lipoproteins are classified as:



HDLs – high-density lipoproteins have more
protein content
LDLs – low-density lipoproteins have a
considerable cholesterol component
VLDLs – very low density lipoproteins are mostly
triglycerides
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Cholesterol
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Figure 24.22
Lipoproteins

The liver is the main source of VLDLs, which
transport triglycerides to peripheral tissues
(especially adipose)

LDLs transport cholesterol to the peripheral tissues
and regulate cholesterol synthesis

HDLs transport excess cholesterol from peripheral
tissues to the liver

Also serve the needs of steroid-producing organs
(ovaries and adrenal glands)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Lipoproteins

High levels of HDL are thought to protect against
heart attack

High levels of LDL, especially lipoprotein (a),
increase the risk of heart attack
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Plasma Cholesterol Levels

The liver produces cholesterol:

At a basal level of cholesterol regardless of dietary
intake

Via a negative feedback loop involving serum
cholesterol levels

In response to saturated fatty acids
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Plasma Cholesterol Levels


Fatty acids regulate excretion of cholesterol

Unsaturated fatty acids enhance excretion

Saturated fatty acids inhibit excretion
Certain unsaturated fatty acids (omega-3 fatty
acids, found in cold-water fish) lower the
proportions of saturated fats and cholesterol
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Non-Dietary Factors Affecting Cholesterol

Stress, cigarette smoking, and coffee drinking
increase LDL levels

Aerobic exercise increases HDL levels

Body shape is correlated with cholesterol levels

Fat carried on the upper body is correlated with
high cholesterol levels

Fat carried on the hips and thighs is correlated with
lower levels
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Body Energy Balance



Bond energy released from catabolized food must
equal the total energy output
Energy intake – equal to the energy liberated
during the oxidation of food
Energy output includes the energy:

Immediately lost as heat (about 60% of the total)

Used to do work (driven by ATP)

Stored in the form of fat and glycogen
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Body Energy Balance

Nearly all energy derived from food is eventually
converted to heat

Cells cannot use this energy to do work, but the
heat:

Warms the tissues and blood

Helps maintain the homeostatic body temperature

Allows metabolic reactions to occur efficiently
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Regulation of Food Intake

When energy intake and energy outflow are
balanced, body weight remains stable

The hypothalamus releases peptides that influence
feeding behavior

Orexins are powerful appetite enhancers

Neuropeptide Y causes a craving for carbohydrates

Galanin produces a craving for fats

GLP-1 and serotonin make us feel full and satisfied
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Feeding Behaviors

Feeding behavior and hunger depend on one or
more of five factors

Neural signals from the digestive tract

Bloodborne signals related to the body energy
stores

Hormones, body temperature, and psychological
factors
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Nutrient Signals Related to Energy Stores

High plasma levels of nutrients that signal
depressed eating

Plasma glucose levels

Amino acids in the plasma

Fatty acids and leptin
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Hormones, Temperature, and Psychological
Factors
 Glucagon and epinephrine stimulate hunger

Insulin and cholecystokinin depress hunger

Increased body temperature may inhibit eating
behavior

Psychological factors that have little to do with
caloric balance can also influence eating behaviors
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Control of Feeding Behavior and Satiety


Leptin, secreted by fat tissue, appears to be the
overall satiety signal

Acts on the ventromedial hypothalamus

Controls appetite and energy output

Suppresses the secretion of neuropeptide Y, a
potent appetite stimulant
Blood levels of insulin and glucocorticoids play a
role in regulating leptin release
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Hypothalamic Command of Appetite
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Figure 24.23
Metabolic Rate


Rate of energy output (expressed per hour) equal to
the total heat produced by:

All the chemical reactions in the body

The mechanical work of the body
Measured directly with a calorimeter or indirectly
with a respirometer
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Metabolic Rate

Basal metabolic rate (BMR)


Reflects the energy the body needs to perform its
most essential activities
Total metabolic rate (TMR)

Total rate of kilocalorie consumption to fuel all
ongoing activities
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Factors that Influence BMR

Surface area, age, gender, stress, and hormones

As the ratio of surface area to volume increases,
BMR increases

Males have a disproportionately high BMR

Stress increases BMR

Thyroxine increases oxygen consumption, cellular
respiration, and BMR
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Regulation of Body Temperature

Body temperature – balance between heat
production and heat loss

At rest, the liver, heart, brain, and endocrine organs
account for most heat production

During vigorous exercise, heat production from
skeletal muscles can increase 30–40 times
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Regulation of Body Temperature

Normal body temperature is 36.2C (98.2F);
optimal enzyme activity occurs at this temperature

Temperature spikes above this range denature
proteins and depress neurons
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Regulation of Body Temperature
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Figure 24.24
Core and Shell Temperature

Organs in the core (within the skull, thoracic, and
abdominal cavities) have the highest temperature

The shell, essentially the skin, has the lowest
temperature

Blood serves as the major agent of heat transfer
between the core and shell

Core temperature remains relatively constant,
while shell temperature fluctuates substantially
(20C–40C)
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Mechanisms of Heat Exchange

Four mechanisms:

Radiation – loss of heat in the form of infrared rays

Conduction – transfer of heat by direct contact

Convection – transfer of heat to the surrounding air


Evaporation – heat loss due to the evaporation of
water from the lungs, mouth mucosa, and skin
(insensible heat loss)
Evaporative heat loss becomes sensible when body
temperature rises and sweating produces increased
water for vaporization
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Role of the Hypothalamus

The main thermoregulation center is the preoptic
region of the hypothalamus

The heat-loss and heat-promoting centers comprise
the thermoregulatory centers

The hypothalamus:

Receives input from thermoreceptors in the skin
and core

Responds by initiating appropriate heat-loss and
heat-promoting activities
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Heat-Promoting Mechanisms

Low external temperature or low temperature of
circulating blood activates heat-promoting centers
of the hypothalamus to cause:

Vasoconstriction of cutaneous blood vessels

Increased metabolic rate

Shivering

Enhanced thyroxine release
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Heat-Loss Mechanisms


When the core temperature rises, the heat-loss
center is activated to cause:

Vasodilation of cutaneous blood vessels

Enhanced sweating
Voluntary measures commonly taken to reduce
body heat include:

Reducing activity and seeking a cooler
environment

Wearing light-colored and loose-fitting clothing
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Skin blood vessels
dilate: capillaries
become flushed with
warm blood; heat
radiates from
skin surface
Activates
heat-loss
center in
hypothalamus
Blood warmer
than hypothalamic
set point
Sweat glands activated:
secrete perspiration, which
is vaporized by body heat,
helping to cool the body
Body temperature decreases:
blood temperature
declines and hypothalamus heat-loss
center “shuts off”
Stimulus:
Stimulus:
Increased body
Decreased body
temperature
temperature (e.g., due
(e.g., when exercising Homeostasis = normal body temperature (35.8°C–38.2°C)to cold environmental
or the climate is hot)
temperatures)
Body temperature increases:
blood temperature
rises and hypothalamus heat-promoting
center “shuts off”
Skin blood vessels constrict:
blood is diverted from skin
capillaries and withdrawn to
deeper tissues; minimizes
overall heat loss
from skin
surface
Skeletal muscles
activated when more
heat must be generated;
shivering begins
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Blood cooler than
hypothalamic set
point
Activates heatpromoting center
in hypothalamus
Figure 24.26
Stimulus:
Increased body
temperature (e.g.,
when exercising or
the climate is hot)
Homeostasis = normal body temperature (35.8°C–38.2°C)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 24.26
Activates
heat-loss
center in
hypothalamus
Blood warmer
than hypothalamic
set point
Stimulus:
Increased body
temperature (e.g.,
when exercising or
the climate is hot)
Homeostasis = normal body temperature (35.8°C–38.2°C)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 24.26
Activates
heat-loss
center in
hypothalamus
Skin blood vessels
dilate: capillaries
become flushed with
warm blood; heat
radiates from skin surface
Blood warmer
than hypothalamic
set point
Stimulus:
Increased body
temperature (e.g.,
when exercising or
the climate is hot)
Homeostasis = normal body temperature (35.8°C–38.2°C)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 24.26
Skin blood vessels
dilate: capillaries
become flushed with
warm blood; heat
radiates from skin surface
Activates
heat-loss
center in
hypothalamus
Blood warmer
than hypothalamic
set point
Stimulus:
Increased body
temperature (e.g.,
when exercising or
the climate is hot)
Sweat glands activated:
secrete perspiration, which
is vaporized by body heat,
helping to cool the body
Body temperature decreases:
blood temperature
declines and hypothalamus heat-loss
center “shuts off”
Homeostasis = normal body temperature (35.8°C–38.2°C)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 24.26
Skin blood vessels
dilate: capillaries
become flushed with
warm blood; heat
radiates from skin surface
Activates
heat-loss
center in
hypothalamus
Blood warmer
than hypothalamic
set point
Stimulus:
Increased body
temperature (e.g.,
when exercising or
the climate is hot)
Sweat glands activated:
secrete perspiration, which
is vaporized by body heat,
helping to cool the body
Body temperature decreases:
blood temperature
declines and hypothalamus heat-loss
center “shuts off”
Homeostasis = normal body temperature (35.8°C–38.2°C)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Stimulus:
Decreased body
temperature (e.g., due
to cold environmental
temperatures)
Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C)
Stimulus:
Decreased body
temperature (e.g., due
to cold environmental
temperatures)
Blood cooler than
hypothalamic set
point
Activates heatpromoting center
in hypothalamus
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C)
Stimulus:
Decreased body
temperature (e.g., due
to cold environmental
temperatures)
Blood cooler than
hypothalamic set
point
Skeletal muscles
activated when more
heat must be generated;
shivering begins
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Activates heatpromoting center
in hypothalamus
Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C)
Skin blood vessels constrict:
blood is diverted from skin
capillaries and withdrawn to
deeper tissues; minimizes
overall heat loss
from skin
surface
Skeletal muscles
activated when more
heat must be generated;
shivering begins
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Stimulus:
Decreased body
temperature (e.g., due
to cold environmental
temperatures)
Blood cooler than
hypothalamic set
point
Activates heatpromoting center
in hypothalamus
Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C)
Skin blood vessels constrict:
blood is diverted from skin
capillaries and withdrawn to
Body temperature increases:
deeper tissues; minimizes
blood temperature
overall heat loss
rises and hypothalafrom skin
mus heat-promoting
surface
center “shuts off”
Skeletal muscles
activated when more
heat must be generated;
shivering begins
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Stimulus:
Decreased body
temperature (e.g., due
to cold environmental
temperatures)
Blood cooler than
hypothalamic set
point
Activates heatpromoting center
in hypothalamus
Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C)
Skin blood vessels constrict:
blood is diverted from skin
capillaries and withdrawn to
Body temperature increases:
deeper tissues; minimizes
blood temperature
overall heat loss
rises and hypothalafrom skin
mus heat-promoting
surface
center “shuts off”
Skeletal muscles
activated when more
heat must be generated;
shivering begins
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Stimulus:
Decreased body
temperature (e.g., due
to cold environmental
temperatures)
Blood cooler than
hypothalamic set
point
Activates heatpromoting center
in hypothalamus
Figure 24.26
Skin blood vessels
dilate: capillaries
become flushed with
warm blood; heat
radiates from
skin surface
Activates
heat-loss
center in
hypothalamus
Blood warmer
than hypothalamic
set point
Sweat glands activated:
secrete perspiration, which
is vaporized by body heat,
helping to cool the body
Body temperature decreases:
blood temperature
declines and hypothalamus heat-loss
center “shuts off”
Stimulus:
Stimulus:
Increased body
Decreased body
temperature
temperature (e.g., due
(e.g., when exercising Homeostasis = normal body temperature (35.8°C–38.2°C)to cold environmental
or the climate is hot)
temperatures)
Body temperature increases:
blood temperature
rises and hypothalamus heat-promoting
center “shuts off”
Skin blood vessels constrict:
blood is diverted from skin
capillaries and withdrawn to
deeper tissues; minimizes
overall heat loss
from skin
surface
Skeletal muscles
activated when more
heat must be generated;
shivering begins
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Blood cooler than
hypothalamic set
point
Activates heatpromoting center
in hypothalamus
Figure 24.26
Hyperthermia

Normal heat loss processes become ineffective and
elevated body temperatures depress the
hypothalamus

This sets up a positive-feedback mechanism,
sharply increasing body temperature and metabolic
rate

This condition, called heat stroke, can be fatal if
not corrected
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Heat Exhaustion

Heat-associated collapse after vigorous exercise,
evidenced by elevated body temperature, mental
confusion, and fainting

Due to dehydration and low blood pressure

Heat-loss mechanisms are fully functional

Can progress to heat stroke if the body is not
cooled and rehydrated
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Fever

Controlled hyperthermia, often a result of
infection, cancer, allergic reactions, or central
nervous system injuries

White blood cells, injured tissue cells, and
macrophages release pyrogens that act on the
hypothalamus, causing the release of
prostaglandins

Prostaglandins reset the hypothalamic thermostat

The higher set point is maintained until the natural
body defenses reverse the disease process
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Developmental Aspects

Good nutrition is essential in utero as well as
throughout life

Lack of proteins needed for fetal growth and in the
first three years of life can lead to mental deficits
and learning disorders

With the exception of insulin-dependent diabetes
mellitus, children free of genetic disorders rarely
exhibit metabolic problems

In later years, non-insulin-dependent diabetes
mellitus becomes a major problem
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Developmental Aspects

Many agents prescribed for age-related medical
problems influence nutrition

Diuretics can cause hypokalemia by promoting
potassium loss

Antibiotics can interfere with food absorption

Mineral oil interferes with absorption of fat-soluble
vitamins

Excessive alcohol consumption leads to
malabsorption problems, certain vitamin and
mineral deficiencies, deranged metabolism, and
damage to the liver and pancreas
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings