Download Nutrition!!!

Nutrition!!!
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Nutrition
Nutrient – a substance that promotes normal
growth, maintenance, and repair
Major nutrients – carbohydrates, lipids, and
proteins
Other nutrients – vitamins, minerals and water
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Carbohydrates
Complex carbohydrates (starches) are all derived
from plants except for lactose (milk) and glycogen
(small amounts from meat)
Simple carbohydrates (sugars) are found in soft
drinks, candy, fruit, and ice cream
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Carbohydrates
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 / 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
Triglycerides: The most abundant dietary lipids
Found in both animal and plant foods
Essential fatty acids – 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:
Helps absorb fat-soluble vitamins
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:
Not used for energy
Component of plasma membranes
A precursor of bile salts & 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
(e.g. one egg yolk)
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Proteins
Animal products:
contain the highest quality of protein
E.g. best ratio of essential amino acids
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
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Proteins: Synthesis and Hydrolysis
All-or-none rule
All amino acids needed must be present at the same
time and in sufficient quantities 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 protein
breakdown and loss
Equal Balance – amount ingested = amount excreted
Positive Balance – synthesis exceeds breakdown
(normal in children and tissue repair)
Negative Balance – breakdown exceeds synthesis (e.g.,
starvation, stress, or injury)
Hormonal control
Anabolic hormones accelerate protein synthesis
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Vitamins
Not used for energy or as building blocks
Function as coenzymes (act w/ an enzyme)
Provided by food, not made in the body
Exceptions: vitamins B & K synthesized by
intestinal bacteria; the conversion of betacarotene to vitamin A in the body
One food item does not contain all the vitamins
needed by the body: need a balanced diet
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Vitamins
Vitamins are either fat soluble or water soluble
Water-soluble vitamins (B-complex and C) are absorbed in
the gastrointestinal tract
Fat-soluble vitamins (A, D, E, and K) bind to ingested
lipids and are absorbed with their digestion products with
B12 additionally requires gastric intrinsic factor to be
absorbed
Vitamins A, D, and E can be stored in the body
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
Make up 4% of total body weight (75% being calcium and
phosphorous)
Calcium, phosphorus, and magnesium salts harden
bone
Sodium and chloride help maintain normal
osmolarity, water balance, and are essential in nerve
and muscle function
Dozens are required in trace amounts
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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 (build up)
Catabolic reactions – hydrolysis of complex
structures into simpler ones (tear down)
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Stages of Metabolism
3 major stages involved in the processing of energycontaining nutrients in the body:
1) Digestion – breakdown of food; nutrients are transported
in blood to tissue cells
2) In cellular cytoplasm, nutrients are either:
A) built into lipids, proteins, or glycogen (anabolic
pathways)
B) broken down by catabolic pathways to pyruvic
acid and acetyl CoA
3) Oxidative breakdown – nutrients are catabolized to
carbon dioxide, water, and ATP
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Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 24.3
Oxidation-Reduction (Redox) Reactions
Oxidation: loss of hydrogen (LEO)
Reduction: gain of hydrogen (GER)
Whenever one substance is oxidized, another
substance is reduced, thus the term Redox rxns.
Oxidized substances lose energy
Reduced substances gain energy
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Oxidation-Reduction (Redox) Reactions
Redox rxns. Are catylized by enzymes
Dehydrogenases: redox rxn. where H+ is
removed
Oxidases: redox rxn. where O2 is transferred
Redox rxns. Require coenzymes from a B vitamin
The coenzyme act as hydrogen (or electron)
acceptor becoming reduced each time a
substrate is oxidized
E.g. nicotinamide adenine dinucleotide
(NAD+) & 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
In the cytoplasm
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Figure 24.4a
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 H+ 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
Outside Mitochondria
Inside Mitochondria
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Figure 24.4b
Carbohydrate (Glucose) 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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First Step: Trapping Glucose
Glucose -6-phosphate
Upon entrance into the cell, glucose is
phosphorylated to Glucose -6-phosphate
Glucose + ATP
This rxn. can not be reversed in most cells thus
trapping “glucose” within the cell
Glucose -6-phosphate + ADP
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Carbohydrate Catabolism
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Figure 24.5
Glycolysis
Occurs in the cytosol and is anaerobic
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
Glycolysis
ATP
Krebs
cycle
ATP
Electron transport chain
and oxidative
phosphorylation
ATP
Glucose
Phase 1
Sugar
activation
Key:
= Carbon
atom
Pi = Inorganic
phosphate
2 ATP
2 ADP
Fructose-1,6bisphosphate
P
P
Phase 2
Sugar
Dihydroxyacetone
cleavage
phosphate
P
Pi
Glyceraldehyde
phosphate
P
2 NAD+
4 ADP
Phase 3
Sugar
oxidation
and formation
of ATP
2 NADH+H+
4 ATP
2 Pyruvic acid
2 NADH+H+
O2
To Krebs
cycle
(aerobic
pathway)
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O2
2 NAD+
2 Lactic acid
Figure 24.6
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Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Glycolysis: Phase 1 and 2
Phase 1: Sugar activation
Two ATP molecules activate glucose into
fructose-1,6-diphosphate
(requires energy investment, e.g. 2 ATP)
Phase 2: Sugar cleavage
Fructose-1,6-bisphosphate is cleaved into two
3-carbon isomers
Dihydroxyacetone 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 4 ATP molecules
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Glycolysis: Phase 3
The final products are:
2 pyruvic acid molecules
2 NADH + H+ molecules (reduced NAD+)
A net gain of 2 ATP / glucose
If O2 is absent, pyruvic acid forms lactic acid and is sent to
the liver
If O2 is present, pyruvic acid enters the Krebs cycle in the
mitochondria and is oxidized to CO2 and H2O
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KU Game Day!!!!
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Krebs Cycle: Preparatory Step
Occurs in the mitochondrial matrix and is fueled
by pyruvic acid and fatty acids
Useful website:
http://www.science.smith.edu/departments/Biology
/Bio231/krebs.html
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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 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
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Cytosol
Pyruvic acid from glycolysis
Glycolysis
ATP
Krebs
cycle
Electron
transport chain
and oxidative
phosphorylation
ATP
NAD+
CO2
CoA
Acetyl CoA
ATP
Oxaloacetic acid
(pickup molecule)
NADH+H+
Mitochondrion
(fluid matrix)
NADH+H+
Citric acid
CoA (initial reactant)
NAD+
Isocitric acid
Malic acid
NAD+
Krebs cycle
CO2
NADH+H+
Fumaric acid
α-Ketoglutaric acid
CO2
FADH2
FAD
Key:
Succinic acid
Succinyl-CoA
CoA
NAD+
NADH+H+
CoA
= Carbon atom
GTP
GDP + Pi
ADP
ATP
Pi = Inorganic phosphate
CoA = Coenzyme A
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Figure 24.7
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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Glycolysis
Krebs
cycle
Electron
transport chain
and oxidative
phosphorylation
ATP
ATP
ATP
H+
H+
H+
H+
Intermembrane
space
Core
Cyt c
e-
eQ
1
3
2
Inner
mitochondrial
membrane
2 H+ +
FADH2
NADH +
H+
(carrying efrom food)
Mitochondrial
matrix
1
2
O2
H2O
FAD
NAD +
ATP
ADP + Pi
H+
Electron Transport Chain
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ATP Synthase
Figure 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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Electron Transport Chain & Oxidative Phosphorylation
Uses O2 directly & occurs in the mitochondria
Uses the reduced coenzymes from the Krebs cycle
as substrates in oxidative phosphorylation rxns.
Useful website:
http://www.science.smith.edu/departments/Biology
/Bio231/etc.html
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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
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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
Summary of ATP Production
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Figure 24.11
Glycogenesis and Glycogenolysis
Cells can not store a lot of ATP
Rising intracellular ATP levels inhibit glucose
catabolism
Glucose is then stored as glycogen or fat
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Glycogenesis and Glycogenolysis
Glycogenesis –
formation of glycogen
from glucose
Glycogenolysis –
breakdown of glycogen
to form glucose
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Figure 24.12
Gluconeogenesis
The process of forming glucose from
noncarbohydrate molecules (glycerol & amino
acids)
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
Energy yield from fat is twice that from glucose or
protein catabolism
Most products of fat metabolism are transported in
lymph as chylomicrons
Lipids in chylomicrons are hydrolyzed by plasma
enzymes and absorbed by cells
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Lipid Metabolism
Catabolism of fats involves two separate pathways
Glycerol pathway
Fatty acids pathway
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Lipid Metabolism
Glycerol is converted to glyceraldehyde phosphate
(yielding 18 ATP / glycerol)
Glyceraldehyde is ultimately converted into acetyl
CoA
Acetyl CoA enters the Krebs cycle
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Lipid Metabolism
Fatty acids undergo beta oxidation in the
mitochondria 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
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Figure 24.13
Lipogenesis
Excess dietary glycerol and fatty acids undergo
lipogenesis to form triglycerides and are stored
Occurs when cellular ATP & glucose levels are
high
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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Lipolysis
Lipolysis, the breakdown of stored fat into glycerol
& fatty acids. Essentially lipogenesis in reverse
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Lipogenesis and Lipolysis
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Figure 24.14
Protein Metabolism: Oxidation of Amino Acids
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
Deamination is the removal of NH2 groups
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Protein Metabolism
The oxidation pathway starts with the removal of
the amino group by transaminase
the amino group is then fed into the urea cycle
The other product of transamidation is pyruvic acid
that enters the citric acid cycle
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Amino Acid Oxidation
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Figure 24.15
Oxidation of Amino Acids
Transamination – switching of an amine group
from an amino acid to a keto acid (usually αketoglutaric 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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Protein Synthesis
Occurs on ribosomes via formation of peptide bonds
Rate of protein synthesis is controlled by hormones
A complete set of amino acids is necessary for protein
synthesis
All essential amino acids must be provided in the diet
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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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
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 adipose tissue:
Glucose and fats are converted and stored as fat
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
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Figure 24.18b
Absorptive State: Carbohydrates
Carbohydrates:
Monosaccharides are delivered to the liver
Fructose & galactose are converted to glucose
Glucose is released to the blood, converted to
glycogen and fat
Glycogen is stored in the liver;
Excess glucose in the blood is stored in muscle as
glycogen or in adipose tissue as fat
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Absorptive State: Triglycerides
Products of fat digestion enter lymph as
chylomicrons
Chylomicrons are hydrolyzed to fatty acids and
glycerol before passing through the capillary wall
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Absorptive State: Amino Acids
Amino acids are delivered to the liver for
deamination
Deaminated amino acids may:
Flow into the Krebs cycle
Are stored as fat in the liver
Are used to synthesize new proteins
However, most amino acids flush through the liver
and remain in the blood for uptake by body cells
for protein synthesis
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Hormonal Control: 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
Glucose oxidation & stimulates its conversion to glycogen
Insulin inhibits: the release of glucose from the liver as well as
gluconeogenesis
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Hormonal Control: Insulin Effects on Metabolism
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Figure 24.19
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
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Figure 24.20a
Postabsorptive State: Sources of Blood
Glucose
Sources of blood glucose: glycogen, protein, fat
1) Glycogenolysis in the liver: 1st line of glucose reserves
2) Glycogenolysis in the skeletal muscle: 2nd line of glucose reserves
3) Lipolysis in adipose tissue & the liver
Glucose is oxidized to pyruvic acid, enters the blood, and is
converted to glucose by the liver and released into the blood
(indirect blood glucose contribution)
Conversion of glycerol to glucose by the liver
4) Catabolism of cellular protein: last line of glucose reserves
Cellular amino acids are deaminated and converted to glucose by
the liver with muscle proteins contributing first
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Principle Pathways in the Postabsorptive
State
Glucose sparing: during post absorptive state, the
brain continues to take up glucose, but all other
organs switch to fatty acids as the major source of
energy sparing glucose for the brain
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Figure 24.20b
Influence of Glucagon
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Figure 24.21
Hormonal and Neural Controls of the
Postabsorptive State
The sympathetic N.S. & several hormones control
the postabsorptive state
Declining blood glucose levels stimulate alpha
cells of the pancreatic islets to produce glucagon
Glucagon targets adipose tissue and liver
The result is increased fatty acid and glycerol
levels in blood
Glucagon is inhibited by rising blood glucose
levels
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Liver Metabolism
Hepatocytes carry out over 500 intricate metabolic
functions
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 & Cholesterol Transport
15% of cholesterol comes from diet, 85% made
from Acetyl CoA by the liver
Not an energy source
Structural source for bile salts, steroid hormones,
and a major component of plasma membranes
Does not circulate in free form in the blood but
rather is transported in bound form by lipoproteins
E.g. HDL, LDL, VLDL
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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).
VLDLs are converted to LDLs
LDLs transport cholesterol to the peripheral tissues
and regulate cholesterol synthesis
HDLs transport excess cholesterol from peripheral
tissues back to the liver where it is broken down
and turned into bile
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Lipoproteins
High levels of HDL are thought to protect against
heart attack
Good: Transported cholesterol is destined for
degradation
High levels of LDL increase the risk of heart attack
Bad: cholesterol is being laid down in the artery
walls
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Plasma Cholesterol Levels
Restriction of dietary cholesterol intake does not
lead to a steep reduction in plasma cholesterol
levels
The liver produces cholesterol:
At a basal level of cholesterol regardless of dietary
intake
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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
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
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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 (or “I’m stuffed!”)
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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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
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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
The younger the person, the higher the BMR
Surprisingly, physical training has little effect on BMR
Body temperature and BMR rise and fall together
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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
As body temperature rises, enzymatic catalysis is
accelerated…to a point
Once above homeostatic range (38-39 °C) neurons
are depressed and proteins begin to denature
Death occurs around 43 °C (109°F)
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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
Heat flows down a thermal gradient (warm to cold)
Body uses four mechanisms of heat transfer:
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 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 (mainly in children)
Results in release of thyroid-stimulating hormone
resulting in release of thyroid hormone which
increases metabolic rate
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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
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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 cytokines (interleukin)
ILs act on the hypothalamus, causing the release of
prostaglandins
Prostaglandins reset the hypothalamic thermostat to a
higher set point than normal temperature
If set too high, brain damage can occur
The higher set point is maintained until the natural body
defenses reverse the disease process (antibiotics also help
this reversal process)
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