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Catabolic Processes
Aerobic: Glucose pyruvate acetyl CoA
Glycolysis
Anaerobic: Glucose Lactate
oxidation
Nitrogen:
-Redistributed if reduced
-Eliminated by urea cycle if excess
Table 1. Catabolic Processes and their Products
AA Catabolism
OBJECTIVES
General Objective:
To explain thoroughly how cells carry out and regulate
complex reaction sequences
Specific Objectives:
1. To be able to differentiate between anabolic and
catabolic pathways
2. To be able to explain briefly how carbohydrates. Lipids,
and proteins are metabolized
3. To be able to correlate relationships between each
pathway
2. Anabolism
- Synthesis of complex organic molecules needed for
cell maintenance, growth and reproduction, i.e.:
Glycogenesis
Gluconeogenesis
Anabolic Processes
Glycogenesis
Glucose Glycogen
Gluconeogenesis
Pyruvate Glucose
Palmitate Biosynthesis
Acetyl CoA Fatty Acids
Non-essential AA
ketoacids
biosynthesis
aminotransferase rxn
Purine & pyrimidine
Nitrogen donors Ring
nucleotide biosynthesis
structures
Protein biosynthesis
Translation
Nucleic Acid biosynthesis
Replication, Transcription
Table 2. Anabolic Processes and their Products
Review:
Catabolic
3. Amphibolic
- Act as links between anabolism and catabolism
- At the crossroad between the 2 pathways, i.e.:
Citric Acid Cycle usually catabolic but
intermediates can be used as precursors of
other rxns
Metabolism includes:
1. Interconversion of chemical compounds within the body
2. Pathways taken by molecules
3. Interrelationships between the pathways
4. Regulating mechanisms
Categories:
1. Catabolism
- Degradation of complex substances to liberate
smaller molecules and energy, i.e.:
Degradation of CHON (protein) to AA (amino
acids)
Triglycerides to FA (fatty acids)
Glucose to Pyruvate
Anabolic
Complex Simple
Simple Complex
(Break down)
(Biosynthesis)
Exergonic
Endergonic
Energy releasing
Energy requiring
Table 3. Catabolic vs. Anabolic Processes
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Glycolysis
- Can occur anaerobically (oxygen absent) but instead of
pyruvate, the product will be lactate
- Linked to oxidative phosphorylation and thus, also
producing ATP
Pentose Phosphate Pathway
- A source of reducing equivalents but instead NADPH is
used for biosynthesis
- Source of ribose for nucleotide and nucleic acid synthesis
- In liver and skeletal muscles: reduction of glutathione
Acyl glycerol (fat) Pathway
- Triose phosphate glycerol moiety of triacylglycerols
Amino Acid Synthesis
- Via pyruvate and/or via intermediates of TCA
Steroid Synthesis
- Acetyl-CoA is a precursor of fatty acids and cholesterol
Glycogenesis
- Formation of glycogen when glucose in in excess
Gluconeogenesis
- Synthesis of glucose from non-carbohydrate sources such
as lactate, amino acids, glycerol
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Fates of Lipids
1. Oxidizes to CO2 and H2O with reducing equivalents
2. Precursor for cholesterol and other steroids
3. Forms ketone bodies (acetoacetate and 3-hydroxybutyrate
[fuels in prolonged fasting])
Dietary Lipids:
Hydrolyzed to monoacylglycerols and fatty acids
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chylomicrons
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40 Hours
Fasting
3.6
1.15
7 Days
starvation
3.5
1.19
Glucose
5.5
Free fatty
0.30
acids
Ketone
Negligible
2.9
4.5
bodies
Table 4. Plasma Concentrations of Metabolic Fuels (mmol/L) in the Fed
and Fasting States (The amount of Ketone bodies (negligible in Fed
State) and Free fatty acids increase as one approaches the starvation
state. The opposite is true for Glucose)
Energy
yield
(kJ/g)
O2
consumed
(L/g)
CO2
produced
(L/g)
RQ (CO2
prod/O2
consumed)
Energy
(kJ/L
O2)
Carbohydrates
Protein
Fat
Alcohol
16
0.829
0.829
1.00
20
17
0.966
0.782
0.81
20
37
2.016
1.427
0.71
20
29
1.429
0.966
0.66
20
Table 5. Energy Yields, Oxygen Consumption, and Carbon Dioxide
Production in the Oxidation of Metabolic Fuels
STARVE-FEED CYCLE
Feed: refers to the intake of meals (the variable fuel input)
after which the fuel is stored (as glycogen and
triacylglycerol) to meet metabolic needs of fasting.
Fed State: glucose as its major fuel; its respiratory
quotient is the ratio of CO2 produced to O2 consumed
o Insulin: controls uptake of glucose in muscle cells
and adipose tissues
o GLUT4: glucose transporter in muscles and
adipose tissues
Fasting State: the metabolic status of a person who has
not eaten overnight; the metabolic state achieved after
complete digestion and absorption of a meal; stimulates
mobilization of the metabolic fuel reserves; raises
circulating glucose
(Source:
http://www.biochem.ucl.ac.uk/~dab/MSc%20clinbioc/MSc%20gluc
ose%20homeostasis.pdf)
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3. Supply of Substrate
ATP or ADP
4. Hormones
Insulin and Glucagon
VII. CLINICAL CORRELATION
Cachexia
- Release of cytokines in response to tumors and other
pathologic conditions
- Happens in prolonged starvation (Harpers)
o Depletion of adipose tissue reserves (increased
metabolic rate)
o Catabolism of muscle tissue and used as fuel (increased
protein catabolism)
Death results when essential tissue proteins are
catabolized and not replaced.
Diabetes Mellitus
- Inability to utilize glucose can either be:
o Receptor resistance to insulin (Type II)
o insulin due to destruction of -cells of pancreas (Type
I)
Hyperglycemic patients
No insulin = gluconeogenesis and lipolysis =
ketogenesis in liver
o In uncontrolled diabetes, ketoacidosis may occur and
lead to coma
o For the fetus, demand for glucose by the fetus +
lactose synthesis in lactation = ketosis
Mild ketosis with hypoglycemia (Harpers)
COMPETENCIES
- Given a normal person, identify biochemical pathways or processes of carbohydrates that are involved to achieve normal growth and
development.
- Apply the biochemical concepts and principles that will help explain the growth and development of the normal person
- Correlate the biochemical or molecular basis with the growth and development of the normal person
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