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Chapter 24B
Nutrition, Metabolism,
Body Temperature
Slides by Barbara Heard and W. Rose.
figures from Marieb & Hoehn 9th ed.
Portions copyright Pearson Education
Protein Metabolism
• Proteins deteriorate, so continually broken
down and replaced
• Amino acids recycled  new proteins or
different compound
• Protein not stored in body
– When dietary protein in excess, amino acids
• Oxidized for energy
• Converted to fat for storage
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Protein Synthesis
• Amino acids most important anabolic
nutrients
– Form all proteins; bulk of functional molecules
• Hormonally controlled
• Requires complete set of amino acids
– Essential amino acids required in diet
• Synthesize 225 – 450 kg protein during
lifetime
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Catabolic-Anabolic Steady State
• Dynamic state in which
– Organic molecules (except DNA) continuously
broken down and rebuilt
– Organs have different fuel preferences
– Uses nutrient pools
• Stores of amino acids, carbohydrates, fats
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Nutrient Pools
• Three interconvertible pools
– Amino acids
– Carbohydrates
– Fats
• Amount and direction of conversion
directed by liver, adipose tissue, skeletal
muscle
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Amino Acid Pool
• Body's total supply of free amino acids
• Proteins lost in urine, hair, skin cells
• Source for
– Resynthesizing body proteins
– Forming amino acid derivatives
– Gluconeogenesis
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Carbohydrate and Fat Pools
• Easily interconverted through key
intermediates
• Differ from amino acid pool
– Fats and carbohydrates oxidized directly to
produce energy; amino acids first converted
to carbohydrate
– Excess carbohydrate and fat can be stored;
amino acids not stored as protein
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Figure 24.17 Interconversion of
carbohydrates, fats, and proteins.
Proteins
Proteins
Carbohydrates
Glycogen
Fats
Triglycerides (neutral fats)
Glucose
Amino acids
Glucose-6-phosphate
Keto acids
Glycerol and fatty acids
Glyceraldehyde 3-phosphate
Pyruvic acid
Lactic acid
Acetyl CoA
Ketone
bodies
Urea
Excreted in urine
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Krebs
cycle
Catabolic-Anabolic Steady State of the Body
• Blood concentrations of energy sources
equalized between absorptive state and
postabsorptive state
– Absorptive state during and 3-5 hours after
each meal; absorption of nutrients occurring
– Postabsorptive state late morning, late
afternoon, all night; GI tract empty; energy
sources supplied by breakdown of reserves
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Absorptive State
• Anabolism exceeds catabolism
• Nutrients stored
• Carbohydrates
– Glucose major cellular energy fuel
– Glucose converted in liver to glycogen or fat
• Synthesized fat + protein released to blood for
storage by adipose tissue as very low density
lipoproteins (VLDLs)
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Absorptive State
• Triglycerides
– Lipoprotein lipase catalyzes lipids of
chylomicrons in muscle and fat tissues
– Most glycerol and fatty acids converted to
triglycerides for storage
– Triglycerides used by adipose tissue, liver,
and skeletal and cardiac muscle as primary
energy source
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Absorptive State
• Amino acids
– Excess amino acids deaminated and used for
ATP synthesis or stored as fat in liver
– Most amino acids used in protein synthesis
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Figure 24.18a Major events and principal metabolic pathways of the absorptive state.
Major metabolic thrust:
anabolism and energy storage
Amino acids
Glucose
Glycerol and
fatty acids
Major energy fuel:
glucose (dietary)
Glucose
Liver metabolism:
amino acids deaminated and
used for energy or stored as fat
Amino acids
Keto acids
Proteins
Glycogen
Triglycerides
Triglycerides
Major events of the absorptive state
© 2013 Pearson Education, Inc.
Figure 24.18b Major events and principal metabolic pathways of the absorptive state.
In all tissues:
In muscle:
Glycogen
Glucose
Gastrointestinal
tract
Glucose
Protein
Glucose
Amino acids
In liver:
Triglycerides
Glycogen
Keto acids
Protein
Fatty
acids
In adipose
tissue:
Glucose
Glyceraldehyde
3-phosphate
Glycerol
Triglycerides
Fatty
acids
Glycerol
Fatty
acids
Triglycerides
Principal pathways of the absorptive state
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Absorptive State: Hormonal Control
• Absorptive state primarily controlled by
insulin
• Insulin secretion stimulated by
– Elevated blood levels of glucose and amino
acids
– Intestinal GIP and parasympathetic
stimulation
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Insulin Effects on Metabolism
• Insulin, a hypoglycemic hormone, enhances
– Facilitated diffusion of glucose into muscle and
adipose cells (brain and liver take up glucose without
insulin)
– Glucose oxidation for energy
– Glycogen and triglyceride formation
– Active transport of amino acids into tissue cells
– Protein synthesis
– Inhibits glucose release from liver, and
gluconeogenesis
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Homeostatic Imbalance
• Diabetes mellitus
– Inadequate insulin production or abnormal
insulin receptors 
– Glucose unavailable to most body cells 
– Blood glucose levels high
– Glucose lost in urine
– Fats and proteins used for energy 
metabolic acidosis, protein wasting, weight
loss
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Postabsorptive State
• Catabolism of fat, glycogen, and proteins
exceeds anabolism
– Net synthesis of fat, glycogen, proteins ends
• Goal - maintain blood glucose between
meals
– Makes glucose available to blood
– Promotes use of fats for energy (glucose
sparing – save glucose for organs that need it
most)
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Sources of Blood Glucose
• Glycogenolysis in liver
• Glycogenolysis in skeletal muscle
• Lipolysis in adipose tissues and liver
– Glycerol used for gluconeogenesis in liver
• Catabolism of cellular protein
– Major source during prolonged fasting
• Amount of fat in body determines how long
can survive without food
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Figure 24.20a Major events and principal metabolic pathways of the postabsorptive state.
Major metabolic thrust:
catabolism and replacement of fuels in blood
Proteins
Glycogen
Triglycerides
Major energy fuels:
glucose provided by glycogenolysis and
gluconeogenesis; fatty acids, and ketones
Glucose
Fatty acids
and ketones
Liver metabolism:
amino acids converted to glucose
Amino acids
Keto acids
Amino
acids
Glucose
Glycerol and
fatty acids
Glucose
Major events of the postabsorptive state
© 2013 Pearson Education, Inc.
Figure 24.20b Major events and principal metabolic pathways of the postabsorptive state.
In adipose
tissue:
Glycogen
2
In muscle:
Protein
4
Triglycerides
Pyruvic and
lactic acids
3
Amino acids
In most tissues:
4
2
Triglycerides 3
In liver:
Glycerol
Amino acids Pyruvic and
lactic acids
4
Keto acids
3
2
Glucose
Fatty
acids +
glycerol
Fatty acids
Ketone
bodies
Keto
acids
Blood glucose
1
Stored
glycogen
(b)
In nervous
tissue:
Principal pathways of the postabsorptive state
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Postabsorptive State: Hormonal and Neural
Controls
• Glucagon - hyperglycemic hormone
– Release stimulated by
• Declining blood glucose
• Rising amino acid levels
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Effects of Glucagon
• Glucagon promotes
– Glycogenolysis and gluconeogenesis in the
liver
– Lipolysis in adipose tissue  fatty acids and
glycerol to blood
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Postabsorptive State: Hormonal and Neural
Controls
• Adipose tissue innervated by sympathetic
nervous system
– Quickly supplies glucose if blood levels low
– Low plasma glucose, fight-or-flight response,
or exercise  fat mobilization and
glycogenolysis
• Initiated by sympathetic nervous system and
epinephrine from adrenal medulla
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Metabolic Role of the Liver
• Hepatocytes
– ~500 metabolic functions
– Process nearly every class of nutrient
– Play major role in regulating plasma
cholesterol levels
– Store vitamins and minerals
– Metabolize alcohol, drugs, hormones, and
bilirubin
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Cholesterol
• Structural basis of bile salts, steroid
hormones, and vitamin D
• Major component of plasma membranes
• 15% of blood cholesterol ingested; rest
made in body, primarily liver
• Lost from body when catabolized or
secreted in bile salts
• Part of hedgehog signaling molecule that
directs embryonic development
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Cholesterol Transport
• Lipoproteins
– Transport water-insoluble cholesterol and
triglycerides in blood
– Regulate lipid entry/exit at target cells
– Contain triglycerides, phospholipids,
cholesterol, and protein
• Higher percentage of lipids  lower density, hence
VLDLs, LDLs, HDLs
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Lipoproteins
• Types of transport lipoproteins
– HDLs (high-density lipoproteins)
• Highest protein content
– LDLs (low-density lipoproteins)
• Cholesterol-rich
– VLDLs (very low-density lipoproteins)
• Mostly triglycerides
– Chylomicrons
• Lowest density
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Figure 24.22 Approximate composition of lipoproteins that transport lipids in body fluids.
From intestine
Made by liver
10%
20%
Returned to
liver
5%
30%
55–65%
80–95%
20%
45%
15–20%
45–50%
10–15%
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25%
3–6%
2–7%
5–10%
1–2%
Chylomicron
VLDL
Triglyceride
Cholesterol
Phospholipid
Proteinl
LDL
HDL
Lipoproteins
• VLDLs
– Transport triglycerides from liver to peripheral tissues
(mostly adipose)
• LDLs
– Transport cholesterol to peripheral tissues for
membranes, storage, or hormone synthesis
• HDLs
– Transport excess cholesterol from peripheral tissues
to liver to be broken down and secreted into bile
– Also provide cholesterol to steroid-producing organs
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Recommended Total Cholesterol, HDL, and
LDL Levels
• Total cholesterol = 200 mg/dl or less
– Levels > 200 mg/dl linked to atherosclerosis
• Form in which cholesterol transported in
blood important to measure
• High HDL thought to protect against heart
disease; >60 good; <40 not good
• High LDL  cholesterol deposits in
vessels; 100 or less good; 130 or above
not good
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Plasma Cholesterol Levels
• The liver produces cholesterol
– At a basal level regardless of dietary
cholesterol intake
– In response to saturated fatty acids
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Plasma Cholesterol Levels
• Ratio of saturated/unsaturated fatty acids
affects blood cholesterol levels
• Saturated fatty acids
– Stimulate liver synthesis of cholesterol
– Inhibit cholesterol excretion from body
• Unsaturated fatty acids
– Enhance excretion of cholesterol
– Enhance cholesterol catabolism to bile salts
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Plasma Cholesterol Levels
• Trans fats
– Healthy oils forced to be solids
• E.g., margarine
– Worse effect on cholesterol levels than
saturated fats
– Increase LDLs and reduce HDLs
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Plasma Cholesterol Levels
• Unsaturated omega-3 fatty acids (found in
cold-water fish)
– Lower proportions of saturated fats and
cholesterol
– Make platelets less sticky  help prevent
spontaneous clotting
– Antiarrhythmic effects on heart
– Lower blood pressure
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Non-Dietary Factors Affecting Cholesterol
• Stress and cigarette smoking lower HDL
levels
• Aerobic exercise and estrogen increase
HDL levels and decrease LDL levels
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Homeostatic Imbalance
• Statins
– Cholesterol-lowering drugs
– Estimated >10 million Americans take statins
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Energy Balance
• Bond energy released from food must
equal total energy output
• Energy intake = energy liberated during
food oxidation
• Energy output
– Immediately lost as heat (~60%)
– Used to do work (driven by ATP)
– Stored as fat or glycogen
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Energy Balance
• Nearly all energy from food eventually
converted to heat - cannot be used to do
work
• Heat energy
– Warms tissues and blood
– Helps maintain homeostatic body temperature
– Allows metabolic reactions to occur efficiently
• If energy intake = energy output – weight
stable
• If not equal – gain or loss of weight
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Obesity
• Body mass index (BMI) = W / H2
(W in kg, H in m)
• Considered overweight if BMI 25 to 30
• Considered obese if BMI greater than 30
– Higher incidence of atherosclerosis, type 2
diabetes mellitus, hypertension, heart
disease, and osteoarthritis
• More adults and children overweight than
20 years ago
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Regulation of Food Intake
• Various nuclei of hypothalamus
– Release peptides  influence feeding behavior
• neuropeptide Y (NPY) enhances appetite
• pro-opiomelanocortin (POMC) and cocaine/amphetamine-regulated transcript (CART) 
suppress appetite
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Regulation of Food Intake
• Feeding behavior and hunger regulated by
–
–
–
–
Neural signals from digestive tract
Bloodborne signals related to body energy stores
Hormones
To lesser extent, body temperature and psychological
factors
• Operate through brain thermoreceptors,
chemoreceptors, and others
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Short-Term Regulation of Food Intake
• Neural signals from GI tract
– High protein content of meal increases and
prolongs afferent vagal signals
– Distension sends signals along vagus nerve
that suppress hunger center
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Short-Term Regulation of Food Intake
• Nutrient signals related to energy stores
– Increased nutrient levels in blood depress
eating
• Rising blood glucose
• Elevated blood amino acid levels
• Blood levels of fatty acids
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Short-Term Regulation of Food Intake
• Hormones
– Gut hormones (e.g., insulin and CCK)
depress hunger
– Glucagon and epinephrine stimulate hunger
– Ghrelin (Ghr) from stomach stimulates
appetite; levels peak prior to mealtime
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Long-Term Regulation of Food Intake
• Leptin
– Hormone secreted by fat cells in response to
increased body fat mass
– Indicator of total energy stores in fat tissue
– Protects against weight loss in times of
nutritional deprivation
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Long-Term Regulation of Food Intake
• Leptin
– Acts on certain neurons in hypothalamus
– Suppresses secretion of NPY which is a
potent appetite stimulant
– Stimulates expression of appetite
suppressants (e.g., CART peptides)
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Leptin
• Rising leptin  some weight loss; not
"magic bullet" for obese patients
• High leptin levels in obese patients;
resistant to its action
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Additional Factors in Regulation of Food
Intake
•
•
•
•
•
Temperature – cold activates hunger
Stress – depends on individual
Psychological factors
Sleep deprivation
Composition of gut bacteria
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Metabolic Rate and Heat Production
• Metabolic rate
– Total heat produced by chemical reactions
and mechanical work of body
– Can be measured
• Directly – calorimeter measures heat liberated
into water chamber
• Indirectly – respirometer measures oxygen
consumption (directly proportional to heat
production)
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Basal Metabolic Rate
• Reflects energy body needs to perform its most
essential activities
• Measured in postabsorptive state (npo 12
hours), reclining position, relaxed mentally and
physically, room temperature 20-25C
• Recorded as kilocalories per square meter of
body surface per hour (kcal/m2/h)
– E.g., 70 kg adult BMR = 66 kcal/h
• Influenced by body surface area, age, gender,
body temperature, stress, thyroxine
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Factors that Influence BMR
• BMR increases as ratio of body surface
area to volume increases
• Decreases with age
• Males have disproportionately higher BMR
• Increases with temperature or stress
• Thyroxine increases oxygen consumption,
cellular respiration, and BMR
• Physical training has little effect on BMR
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Metabolic Rate
• Total metabolic rate (TMR)
– Rate of kilocalorie consumption to fuel all
ongoing activities
– Increases with skeletal muscle activity and
food ingestion (food-induced
thermogenesis)
• Greatest with protein and alcohol ingestion
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Regulation of Body Temperature
• Body temperature reflects balance
between heat production and heat loss
• At rest, liver, heart, brain, kidneys,
endocrine organs generate most heat
• During exercise, heat production from
skeletal muscles increases dramatically
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Regulation of Body Temperature
• Normal body temperature = 37C  5C
(98.6F)
– Optimal enzyme activity at this temperature
• Increased temperature denatures proteins
and depresses neurons
– Children <5  convulsions at 41C(106F)
– ~43C (109F) - limit for life
• Tissues tolerate low body temperatures
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Core and Shell Temperature
• Core (organs within skull, thoracic &
abdominal cavities) has highest
temperature
– Rectal temperature best clinical indicator
• Core temperature regulated; fairly
constant
– Blood - major agent of heat exchange
between core and shell
• Shell (skin) – lowest temperature
– Fluctuates between 20C – 40C
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Mechanisms of Heat Exchange
• Four mechanisms of heat transfer
– Radiation - loss of heat by infrared rays
– Conduction - transfer of heat by direct
contact
– Convection - transfer of heat to surrounding
air
– Evaporation - heat loss due to evaporation of
water from body surfaces
• Heat absorbed by water during evaporation – heat
of vaporization
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Mechanisms of Heat Exchange
• Insensible heat loss accompanies
insensible water loss from lungs, oral
mucosa, and skin
– Loss ~ 10% of basal heat production
• Sensible heat loss – when body
temperature rises and sweating increases
water vaporization
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Role of the Hypothalamus
• Hypothalamus receives afferent input from
– Peripheral thermoreceptors in shell (skin)
– Central thermoreceptors (some in
hypothalamus) in core
• Initiates appropriate heat-loss and heatpromoting activities
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Heat-Promoting Mechanisms
• Constriction of cutaneous blood vessels
– Sympathetic nervous system stimulates
• Shivering – heat from skeletal muscle
activity
• Increased metabolic rate via epinephrine
and norepinephrine
– Chemical (nonshivering) thermogenesis infants
– Brown adipose tissue in adults
• Enhanced thyroxine release - infants
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Heat-Promoting Mechanisms
• Behavioral modifications (voluntary)
measures include
– Putting on more clothing
– Drinking hot fluids
– Changing posture (clasping arms across
chest)
– Increasing physical activity (jumping up and
down)
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Heat-Loss Mechanisms
•
•
•
•
Heat-promoting center inhibited
Dilation of cutaneous blood vessels
Enhanced sweating
Voluntary measures include
– Reducing activity and seeking a cooler
environment
– Wearing light-colored, loose-fitting clothing
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Homeostatic Imbalance
• Hyperthermia
– Elevated body temperature depresses
hypothalamus
– Positive-feedback mechanism (heat stroke)
begins at core temperature of 41C 
increased temperatures
• Skin hot and dry; organs damaged
– Can be fatal if not corrected
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Homeostatic Imbalance
• Heat exhaustion
– Heat-associated collapse after vigorous
exercise
– Due to dehydration and low blood pressure
– Heat-loss mechanisms still functional
– May progress to heat stroke if not cooled and
rehydrated promptly
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Homeostatic Imbalance
• Hypothermia
– Low body temperature from cold exposure
• Vital signs decrease
– Shivering stops at core temperature of
30 - 32C
– Can progress to coma and death by cardiac
arrest at ~ 21C
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Fever
• Controlled hyperthermia
• Due to infection (also cancer, allergies, or
CNS injuries)
• Macrophages release cytokines (also
called pyrogens)
– Cause release of prostaglandins from
hypothalamus
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Fever
• Prostaglandins reset hypothalamic
thermostat higher
–  heat-producing mechanisms – temperature
rises
• Natural body defenses or antibiotics
reverse disease process
– Cryogens (e.g., vasopressin) reset thermostat
to lower (normal) level  heat-loss
mechanisms  temperature falls
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