1. Glycolysis: Phase 1 and 2 Phase 1: Sugar activation
two ATP molecules used to activate glucose into:
fructose-1,6-diphosphate
Phase 2: Sugar cleavage
Fructose-1,6-bisphosphate is cleaved into:
two 3-carbon isomers
Phase 3: Oxidation and ATP formation
3-carbon sugars are oxidized (reducing NAD+)
ATP is formed by substrate-level phosphorylation

2. Glycolysis Figure 24.6 Glucose Key: Phase 1 Sugar activation 2 ATP
Krebs
cycle
Electron trans-
port chain
and oxidative
phosphorylation
ATP
ATP
ATP
Glucose
Key:
Phase 1
Sugar
activation
2 ATP
= Carbon
atom
2 ADP Pi
= Inorganic
phosphate
Fructose-1,6-
bisphosphate P P
Phase 2
Sugar
cleavage
Dihydroxyacetone
phosphate
Glyceraldehyde
phosphate P P Pi
2 NAD+
4 ADP 2
NADH+H+
4 ATP
Phase 3
Sugar
oxidation
and formation
of ATP
2 Pyruvic acid 2
NADH+H+ O2 O2
2 NAD+
To Krebs
cycle
(aerobic
pathway)
2 Lactic acid
Figure 24.6

3. The final products of glycolysis:
Glycolysis: Phase 3
The final products of glycolysis:
Two pyruvic acid molecules
Two NADH + H+ molecules (reduced NAD+)
A net gain of two ATP molecules (4ATP- 2ATP)

4. Krebs Cycle: Preparatory Step
Occurs inside the mitochondria in the mitochondrial matrix
Fueled by:
Pyruvic acid (carbohydrates)
Fatty acids (lipids)
Pyruvic acid is converted to acetyl CoA in three main steps:
Decarboxylation
Carbon is removed from pyruvic acid
Carbon dioxide is released

5. Krebs Cycle: Preparatory Step
Oxidation
Hydrogen atoms are removed from pyruvic acid
NAD+ accepts the H2 atoms and is reduced to NADH + H+
Formation of acetyl CoA
Decarboxylation results in acetic acid formation
Acetci acid combines with Co A
Acetyl CoA is formed

6. Each molecule of glucose entering glycolysis, results in:
Krebs Cycle
A cycle of eight steps 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
Each molecule of glucose entering glycolysis, results in:
Two molecules of acetyl CoA entering the Krebs cycle

7. Figure 24.7 Pyruvic acid from glycolysis Cytosol CO2 NAD+ CoA NADH+H+
Electron
transport chain
and oxidative
phosphorylation
Krebs
cycle
CO2
NAD+
CoA
NADH+H+
Mitochondrion
(fluid matrix)
Acetyl CoA
ATP
ATP
ATP
Oxaloacetic acid
Citric acid
NADH+H+
(pickup molecule)
CoA
(initial reactant)
NAD+
Malic acid
Isocitric acid
NAD+
Krebs cycle
CO2
NADH+H+
Fumaric acid
a-Ketoglutaric acid
CoA
CO2
FADH2
NAD+
Succinic acid
Succinyl-CoA
NADH+H+
FAD
Key:
CoA
= Carbon atom
GTP
GDP + Pi Pi
= Inorganic phosphate
CoA
= Coenzyme A
ADP
ATP
Figure 24.7

8. Electron Transport Chain
The released hydrogens from glucose oxidation:
Are transported by coenzymes NADH and FADH2
Enter a chain of proteins
Combine with molecular oxygen to form water
Release energy
Energy released is harnessed to:
Attach inorganic phosphate groups (Pi) to ADP
Making ATP by oxidative phosphorylation

9. Mechanism of Oxidative Phosphorylation
hydrogens delivered to the chain are split into:
Protons (H+) and electrons
Protons are pumped across
Inner mitochondrial membrane
Electrons are shuttled from:
One acceptor to the next

10. 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
Energy is used to bond inorganic phosphate (Pi) to ADP producing ATP

11. Summary of ATP Production
Figure 24.11

12. Glycogenesis and Glycogenolysis
Formation of glycogen
When glucose supplies exceed cellular need for ATP synthesis
Glycogenolysis:
Breakdown of glycogen
In response to low blood glucose
Figure 24.12

13. Formation of sugar from non-carbohydrate molecules
Gluconeogenesis
Formation of sugar from non-carbohydrate molecules
Takes place mainly in the liver
Protects the body, especially the brain:
From damaging effects of hypoglycemia
By ensuring ATP synthesis can continue

14. Pancraatic lipases digestion of lipids results in:
Lipid Metabolism
Pancraatic lipases digestion of lipids results in:
Free fatty acids (FFA)
Monoglycerides
Glycerol
FFA & monoglycerides are water insoluble
They quickly associate with:
Bile salts (Polar & non-polar faces)
Lecithin (phospholipid)
This association forms micelles

15. Micelles reach epithelial surface (between microvilli)
Lipid Metabolism
Micelles reach epithelial surface (between microvilli)
Their content leave and diffuse thru plasma membrane
Inside epith. cell (sER) triglycerides are resynthesized
Triglycerides combine with:
Lecithin, other phospholipids, cholesterol
Combination is then coated with protein forming chylomicrons (H2O soluble lipoprotein)
Chylomicrons (too big) leave epith. cells by exocytosis
They enter lacteals (more permeable) & transported as lymph
They join the venous blood thru the thoracic duct

16. Lipid Metabolism
Triglycerides in chylomicrons are hydrolyzed to fatty acids & glycerol
Hydrolysis is achieved by the enzyme lipoprotein lipase
This enzyme is associated with the capillary endo- thelium of the liver & adipose tissue
The resulting fatty acids & glycerol can then pass thru the capillary walls to be used by tissue cells
Residual chylomicron is made into new lipoprotein by the liver cells & used in colesterol transport
Only neutral fats are routinely oxidized for energy

17. Catabolism of fats involves two separate pathways
Lipid Metabolism
Catabolism of fats involves two separate pathways
Glycerol pathway
Fatty acids pathway
Glycerol is converted to:
Glyceraldehyde phosphate (GP)
GP is converted into acetyl CoA
Acetyl CoA enters the Krebs cycle
Energy (ATP) is produced

18. Fatty acids undergo β-oxidation, which produces:
Lipid Metabolism
Fatty acids undergo β-oxidation, which produces:
Two-carbon acetic acid fragments
These fragments enter the Krebs cycle
The resulting reduced coenzymes enter the electron transport chain
Energy (ATP) is produced
Short chain fatty acid from fat breakdown:
Don not follow the pathway described above
Simply diffuse into portal blood & be distributed

19. Lipid Metabolism
Figure 24.13

20. Lipogenesis and Lipolysis
Conversion of excess dietary glycerol and fatty acids into triglycerides
Glucose is easily converted into fat since acetyl CoA is:
An intermediate in glucose catabolism
The starting molecule for fatty acid synthesis

21. Lipogenesis and Lipolysis
The breakdown of stored fat
Is essentially lipogenesis in reverse

22. Excess dietary protein results in:
Protein Metabolism
Excess dietary protein results in:
Amino acids oxidation for energy
Convertion of amino acids into fat for storage
Amino acids must be:
Deaminated prior to oxidation for energy
Deaminated amino acids are converted into:
Pyruvic acid, or
One of the intermediate keto acids
These acids are intermediates in the Krebs cycle

23. A brief summary of liver functions:
Packages fatty acids to be stored and transported
Synthesizes plasma proteins
Forms nonessential amino acids
Converts deamination ammonia into urea
Stores glucose as glycogen
Regulates blood glucose homeostasis
Stores vitamins,
Detoxifies substances

24. Is the structural basis of:
Cholesterol
Is the structural basis of:
Bile salts
Steroid hormones, and
Vitamin D
Transported :
To and from tissues via lipoproteins

25. Lipoproteins are classified as:
Cholesterol
Lipoproteins are classified as:
HDLs (Healthy cholesterol):
High-density lipoproteins
Have more protein content
LDLs (Lethal cholesterol):
Low-density lipoproteins
Have a considerable cholesterol component
VLDLs:
Very low density lipoproteins
Are mostly triglycerides

26. Cholesterol
Figure 24.22

27. Lipoproteins High levels of HDL: High levels of LDL:
Thought to protect against heart attack
High levels of LDL:
Increase the risk of heart attack

28. Plasma Cholesterol Levels
The liver produces cholesterol:
At a basal level regardless of dietary intake
Via a negative feedback loop involving low serum cholesterol levels
In response to saturated fatty acids (stimulate synthesis & inhibit excretion)

29. Regulation of Body Temperature
Balance between heat production and heat loss
At rest, most heat production is accounted for by:
Liver, heart, brain, and endocrine organs
During vigorous exercise:
Heat production from skeletal muscles can increase 30–40 times

30. Regulation of Body Temperature
Normal body temperature:
Averages 37 C (98.6F)
Ranges C (96-101F)
Fluctuates 1C (1.8F) /24hrs (morning vs evening)
Optimal enzyme activity occurs at this temperature
Temperature spikes above this range:
Denature proteins
Depress neurons

31. Core and Shell Temperature
Core organs (have the highest temperature) are found:
Within the skull
Thoracic cavity
Abdominal cavity
The shell (has the lowest temperature) :
Essentially the skin
Major agent of heat transfer between the core and shell:
Blood
Core temperature:
Remains relatively constant
Shell temperature:
Fluctuates substantially (20–40C)

32. 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
Skin

33. Heat-Promoting Mechanisms
Stimuli:
Low external temperature
Low temperature of circulating blood
Heat-promoting centers (hypothalamus) cause:
Vasoconstriction of cutaneous blood vessels
Increased metabolic rate
Shivering
Enhanced thyroxine release

34. Heat-loss center is activated to cause:
Heat-Loss Mechanisms
Stimulus:
Core temperature rises:
Heat-loss center is activated to cause:
Vasodilation of cutaneous blood vessels
Enhanced sweating
Voluntary measures to reduce body heat:
Reduce activity
Seek a cooler environment
Wear light-colored & loose-fitting clothing