Chapter 24: Nutrition, Metabolism, and Temperature

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Transcript Chapter 24: Nutrition, Metabolism, and Temperature

Nutrition, Metabolism,
and Body Temperature
Regulation
24
Part A
Chapter 24: Nutrition, Metabolism, and
Temperature
1
Nutrition
 Nutrient – a substance that promotes normal growth,
maintenance, and repair
 Major nutrients – carbohydrates, lipids, and proteins
 Other nutrients – vitamins and minerals (and
technically speaking, water)
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Nutrition
Chapter 24: Nutrition, Metabolism, and
Temperature
Figure
24.1
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Carbohydrates
 Complex carbohydrates (starches) are found in
bread, cereal, flour, pasta, nuts, and potatoes
 Simple carbohydrates (sugars) are found in soft
drinks, candy, fruit, and ice cream
 Glucose is the molecule ultimately used by body
cells to make ATP
 Neurons and RBCs rely almost entirely upon
glucose to supply their energy needs
 Excess glucose is converted to glycogen or fat and
stored
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Carbohydrates
 The minimum amount of carbohydrates needed to
maintain adequate blood glucose levels is 100 grams
per day
 Starchy foods and milk have nutrients such as
vitamins and minerals in addition to complex
carbohydrates
 Refined carbohydrate foods (candy and soft drinks)
provide energy sources only and are referred to as
“empty calories”
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Lipids
 The most abundant dietary lipids, triglycerides, are found in
both animal and plant foods
 Essential fatty acids – linoleic and linolenic acid, found in
most vegetables, must be ingested
 Dietary fats:
 Help the body to absorb vitamins
 Are a major energy fuel of hepatocytes and skeletal muscle
 Are a component of myelin sheaths and all cell membranes
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Lipids
 Fatty deposits in adipose tissue provide:
 A protective cushion around body organs
 An insulating layer beneath the skin
 An easy-to-store concentrated source of energy
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Lipids
 Prostaglandins function in:
 Smooth muscle contraction
 Control of blood pressure
 Inflammation
 Cholesterol stabilizes membranes and is a precursor
of bile salts and steroid hormones
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Lipids: Dietary Requirements
 Higher for infants and children than for adults
 The American Heart Association suggests that:
 Fats should represent less than 30% of one’s total
caloric intake
 Saturated fats should be limited to 10% or less of
one’s total fat intake
 Daily cholesterol intake should not exceed 200 mg
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Proteins
 Complete proteins that meet all the body’s amino
acid needs are found in eggs, milk, milk products,
meat, and fish
 Incomplete proteins are found in legumes, nuts,
seeds, grains, and vegetables
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Proteins
 Proteins supply:
 Essential amino acids, the building blocks for
nonessential amino acids
 Nitrogen for nonprotein nitrogen-containing
substances
 Daily intake should be approximately 0.8g/kg of
body weight
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Proteins: Synthesis and Hydrolysis
 All-or-none rule
 All amino acids needed must be present at the same
time for protein synthesis to occur
 Adequacy of caloric intake
 Protein will be used as fuel if there is insufficient
carbohydrate or fat available
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Proteins: Synthesis and Hydrolysis
 Nitrogen balance
 The rate of protein synthesis equals the rate of
breakdown and loss
 Positive – synthesis exceeds breakdown (normal in
children and tissue repair)
 Negative – breakdown exceeds synthesis (e.g.,
stress, burns, infection, or injury)
 Hormonal control
 Anabolic hormones accelerate protein synthesis
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Vitamins
 Organic compounds needed for growth and good
health
 They are crucial in helping the body use nutrients
and often function as coenzymes
 Only vitamins D, K, and B are synthesized in the
body; all others must be ingested
 Water-soluble vitamins (B-complex and C) are
absorbed in the gastrointestinal tract
 B12 additionally requires gastric intrinsic factor to
be absorbed
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Vitamins
 Fat-soluble vitamins (A, D, E, and K) bind to
ingested lipids and are absorbed with their digestion
products
 Vitamins A, C, and E also act in an antioxidant
cascade
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Minerals
 Seven minerals are required in moderate amounts
 Calcium, phosphorus, potassium, sulfur, sodium,
chloride, and magnesium
 Dozens are required in trace amounts
 Minerals work with nutrients to ensure proper body
functioning
 Calcium, phosphorus, and magnesium salts harden
bone
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Minerals
 Sodium and chloride help maintain normal
osmolarity, water balance, and are essential in nerve
and muscle function
 Uptake and excretion must be balanced to prevent
toxic overload
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Metabolism
 Metabolism – all chemical reactions necessary to
maintain life
 Cellular respiration – food fuels are broken down
within cells and some of the energy is captured to
produce ATP
 Anabolic reactions – synthesis of larger molecules
from smaller ones
 Catabolic reactions – hydrolysis of complex
structures into simpler ones
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Metabolism
 Enzymes shift the high-energy phosphate groups of
ATP to other molecules
 These phosphorylated molecules are activated to
perform cellular functions
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Stages of Metabolism
 Energy-containing nutrients are processed in three
major stages
 Digestion – breakdown of food; nutrients are
transported to tissues
 Anabolism and formation of catabolic intermediates
where nutrients are:
 Built into lipids, proteins, and glycogen
 Broken down by catabolic pathways to pyruvic
acid and acetyl CoA
 Oxidative breakdown – nutrients are catabolized to
carbon dioxide, water, and ATP
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Stages of Metabolism
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Figure
24.3
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Oxidation-Reduction (Redox) Reactions
 Oxidation occurs via the gain of oxygen or the loss
of hydrogen
 Whenever one substance is oxidized, another
substance is reduced
 Oxidized substances lose energy
 Reduced substances gain energy
 Coenzymes act as hydrogen (or electron) acceptors
 Two important coenzymes are nicotinamide adenine
dinucleotide (NAD+) and flavin adenine dinucleotide
(FAD)
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Mechanisms of ATP Synthesis:
Substrate-Level Phosphorylation
 High-energy
phosphate groups
are transferred
directly from
phosphorylated
substrates to ADP
 ATP is synthesized
via substrate-level
phosphorylation in
glycolysis and the
Krebs cycle
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Figure
24.4a
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Mechanisms of ATP Synthesis:
Oxidative Phosphorylation
 Uses the chemiosmotic process whereby the
movement of substances across a membrane is
coupled to chemical reactions
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Mechanisms of ATP Synthesis:
Oxidative Phosphorylation
 Is carried out by the electron transport proteins in
the cristae of the mitochondria
 Nutrient energy is used to pump hydrogen ions into
the intermembrane space
 A steep diffusion gradient across the membrane
results
 When hydrogen ions flow back across the
membrane through ATP synthase, energy is
captured and attaches phosphate groups to ADP (to
make ATP)
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Mechanisms of ATP Synthesis:
Oxidative Phosphorylation
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Figure
24.4b
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Carbohydrate Metabolism
 Since all carbohydrates are transformed into
glucose, it is essentially glucose metabolism
 Oxidation of glucose is shown by the overall
reaction:
C6H12O6 + 6O2  6H2O + 6CO2 + 36 ATP + heat
 Glucose is catabolized in three pathways
 Glycolysis
 Krebs cycle
 The electron transport chain and oxidative
phosphorylation
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Carbohydrate Catabolism
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Figure
24.5
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Glycolysis
 A three-phase pathway in which:
 Glucose is oxidized into pyruvic acid
 NAD+ is reduced to NADH + H+
 ATP is synthesized by substrate-level
phosphorylation
 Pyruvic acid:
 Moves on to the Krebs cycle in an aerobic pathway
 Is reduced to lactic acid in an anaerobic
environment
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Glycolysis
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Figure 24.6
Glycolysis: Phase 1 and 2
 Phase 1: Sugar activation
 Two ATP molecules activate glucose into
fructose-1,6-diphosphate
 Phase 2: Sugar cleavage
 Fructose-1,6-bisphosphate is cleaved into two
3-carbon isomers
 Bishydroxyacetone phosphate
 Glyceraldehyde 3-phosphate
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Glycolysis: Phase 3
 Phase 3: Oxidation and ATP formation
 The 3-carbon sugars are oxidized (reducing NAD+)
 Inorganic phosphate groups (Pi) are attached to
each oxidized fragment
 The terminal phosphates are cleaved and captured
by ADP to form four ATP molecules
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Glycolysis: Phase 3
 The final products are:
 Two pyruvic acid molecules
 Two NADH + H+ molecules (reduced NAD+)
 A net gain of two ATP molecules
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Krebs Cycle: Preparatory Step
 Occurs in the mitochondrial matrix and is fueled by
pyruvic acid and fatty acids
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Krebs Cycle: Preparatory Step
 Pyruvic acid is converted to acetyl CoA in three
main steps:
 Decarboxylation
 Carbon is removed from pyruvic acid
 Carbon dioxide is released
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Krebs Cycle: Preparatory Step
 Oxidation
 Hydrogen atoms are removed from pyruvic acid
 NAD+ is reduced to NADH + H+
 Formation of acetyl CoA – the resulting acetic acid
is combined with coenzyme A, a sulfur-containing
coenzyme, to form acetyl CoA
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Krebs Cycle
 An eight-step cycle in which each acetic acid is
decarboxylated and oxidized, generating:
 Three molecules of NADH + H+
 One molecule of FADH2
 Two molecules of CO2
 One molecule of ATP
 For each molecule of glucose entering glycolysis,
two molecules of acetyl CoA enter the Krebs cycle
PLAY
Krebs Cycle
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Krebs Cycle
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Figure
Electron Transport Chain
 Food (glucose) is oxidized and the released
hydrogens:
 Are transported by coenzymes NADH and FADH2
 Enter a chain of proteins bound to metal atoms
(cofactors)
 Combine with molecular oxygen to form water
 Release energy
 The energy released is harnessed to attach inorganic
phosphate groups (Pi) to ADP, making ATP by
oxidative phosphorylation
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Mechanism of Oxidative Phosphorylation
 The hydrogens delivered to the chain are split into
protons (H+) and electrons
 The protons are pumped across the inner
mitochondrial membrane by:
 NADH dehydrogenase (FMN, Fe-S)
 Cytochrome b-c1
 Cytochrome oxidase (a-a3)
 The electrons are shuttled from one acceptor to the
next
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Mechanism of Oxidative Phosphorylation
 Electrons are delivered to oxygen, forming oxygen
ions
 Oxygen ions attract H+ to form water
 H+ pumped to the intermembrane space:
 Diffuses back to the matrix via ATP synthase
 Releases energy to make ATP
PLAY
InterActive Physiology®:
Muscular System: Muscular Metabolism
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Mechanism of Oxidative Phosphorylation
Chapter 24: Nutrition, Metabolism, and
Temperature
Figure
42 24.8
Electronic Energy Gradient
 The transfer of energy from NADH + H+ and
FADH2 to oxygen releases large amounts of energy
 This energy is released in a stepwise manner
through the electron transport chain
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Electronic Energy Gradient
 The electrochemical proton gradient across the inner
membrane:
 Creates a pH gradient
 Generates a voltage gradient
 These gradients cause H+ to flow back into the
matrix via ATP synthase
PLAY
Electron Transport
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Electronic Energy Gradient
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Figure
24.9
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ATP Synthase
 The enzyme consists of three parts: a rotor, a knob,
and a rod
 Current created by H+ causes the rotor and rod to
rotate
 This rotation activates catalytic sites in the knob
where ADP and Pi are combined to make ATP
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Structure of ATP Synthase
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Figure
24.10
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Summary of ATP Production
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Figure
24.11
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Glycogenesis and Glycogenolysis
 Glycogenesis –
formation of
glycogen when
glucose supplies
exceed cellular need
for ATP synthesis
 Glycogenolysis –
breakdown of
glycogen in
response to low
blood glucose
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Figure 24.12
Gluconeogenesis
 The process of forming sugar from noncarbohydrate
molecules
 Takes place mainly in the liver
 Protects the body, especially the brain, from the
damaging effects of hypoglycemia by ensuring ATP
synthesis can continue
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Lipid Metabolism
 Most products of fat metabolism are transported in
lymph as chylomicrons
 Lipids in chylomicrons are hydrolyzed by plasma
enzymes and absorbed by cells
 Only neutral fats are routinely oxidized for energy
 Catabolism of fats involves two separate pathways
 Glycerol pathway
 Fatty acids pathway
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Lipid Metabolism
 Glycerol is converted to glyceraldehyde phosphate
 Glyceraldehyde is ultimately converted into acetyl
CoA
 Acetyl CoA enters the Krebs cycle
 Fatty acids undergo beta oxidation which produces:
 Two-carbon acetic acid fragments, which enter the
Krebs cycle
 Reduced coenzymes, which enter the electron
transport chain
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Lipid Metabolism
Chapter 24: Nutrition, Metabolism, and
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Figure
24.13
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Lipogenesis and Lipolysis
 Excess dietary glycerol and fatty acids undergo
lipogenesis to form triglycerides
 Glucose is easily converted into fat since acetyl CoA
is:
 An intermediate in glucose catabolism
 The starting molecule for the synthesis of fatty
acids
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Lipogenesis and Lipolysis
 Lipolysis, the breakdown of stored fat, is essentially
lipogenesis in reverse
 Oxaloacetic acid is necessary for the complete
oxidation of fat
 Without it, acetyl CoA is converted into ketones
(ketogenesis)
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Lipogenesis and Lipolysis
Chapter 24: Nutrition, Metabolism, and
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Figure
24.14
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Lipid Metabolism:
Synthesis of Structural Materials
 Phospholipids are important components of myelin
and cell membranes
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Lipid Metabolism:
Synthesis of Structural Materials
 The liver:
 Synthesizes lipoproteins for transport of cholesterol
and fats
 Makes tissue factor, a clotting factor
 Synthesizes cholesterol for acetyl CoA
 Uses cholesterol to form bile salts
 Certain endocrine organs use cholesterol to
synthesize steroid hormones
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Protein Metabolism
 Excess dietary protein results in amino acids being:
 Oxidized for energy
 Converted into fat for storage
 Amino acids must be deaminated prior to oxidation
for energy
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Protein Metabolism
 Deaminated amino acids are converted into:
 Pyruvic acid
 One of the keto acid intermediates of the Krebs
cycle
 These events occur as transamination, oxidative
deamination, and keto acid modification
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Nutrition, Metabolism,
and Body Temperature
Regulation
24
Part B
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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
Chapter 24: Nutrition, Metabolism, and
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Table
24.2.1
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Summary: Lipid and Protein Metabolic
Reactions
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Table
24.2.2
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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
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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
Chapter 24: Nutrition, Metabolism, and
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Figure
24.17
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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
Chapter 24: Nutrition, Metabolism, and
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Figure
24.18a
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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
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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
Chapter 24: Nutrition, Metabolism, and
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Figure
24.18b
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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
 Insulin enhances:
 Active transport of amino acids into tissue cells
 Facilitated diffusion of glucose into tissue
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Insulin Effects on Metabolism
Chapter 24: Nutrition, Metabolism, and
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Figure
24.19
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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
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Postabsorptive State
Chapter 24: Nutrition, Metabolism, and
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Figure
24.20a
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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)
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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
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Principle Pathways in the Postabsorptive State
Chapter 24: Nutrition, Metabolism, and
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Figure
24.20b
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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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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
Chapter 24: Nutrition, Metabolism, and
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Figure
24.22
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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)
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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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Control of Feeding Behavior and Satiety
Chapter 24: Nutrition, Metabolism, and
Temperature
Figure
24.23
106
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
 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
Chapter 24: Nutrition, Metabolism, and
Temperature
Figure
24.25
111
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
 The body uses four mechanisms of heat exchange
 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
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Mechanisms of Body Temperature Regulation
Chapter 24: Nutrition, Metabolism, and
Temperature
Figure
24.27
117
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
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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
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