This document provides information on beta-oxidation of fatty acids. It discusses the three stages of beta-oxidation: activation of fatty acids in the cytosol, transport into mitochondria via carnitine shuttle, and beta-oxidation in the mitochondrial matrix. The four reactions of each beta-oxidation cycle are also described: oxidation, hydration, oxidation, and cleavage. Deficiencies in beta-oxidation can cause conditions like sudden infant death syndrome.
Pentose phosphate pathway is also called Hexose monophosphate pathway/ HMP shunt/ Phosphogluconate pathway.
It is an alternative route for the metabolism of glucose.
It is more complex pathway than glycolysis.
It is more anabolic in nature.
It takesplace in cytosol.
The tissues such as liver, adipose tissue, adrenal gland, erythrocytes,testes and lactating mammary gland are highly active in HMP shunt.
It concern with the biosynthesis of NADPH and pentoses.
Pentose phosphate pathway is also called Hexose monophosphate pathway/ HMP shunt/ Phosphogluconate pathway.
It is an alternative route for the metabolism of glucose.
It is more complex pathway than glycolysis.
It is more anabolic in nature.
It takesplace in cytosol.
The tissues such as liver, adipose tissue, adrenal gland, erythrocytes,testes and lactating mammary gland are highly active in HMP shunt.
It concern with the biosynthesis of NADPH and pentoses.
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
De novo synthesis of fatty acids (Biosynthesis of fatty acids)Ashok Katta
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Glycolysis (from glycose, an older term for glucose + -lysis degradation) is the metabolic pathway that converts glucose C6H12O6, into pyruvate, CH3COCOO− + H+. The free energy released in this process is used to form the high-energy molecules ATP (adenosine triphosphate) and NADH (reduced nicotinamide adenine ...
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
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Synthesis of fatty acids in the body. Detailed pathway for de novo synthesis of fatty acids in the body including its energetic and regulation. also cover Multienzyme complex
Glycolysis (from glycose, an older term for glucose + -lysis degradation) is the metabolic pathway that converts glucose C6H12O6, into pyruvate, CH3COCOO− + H+. The free energy released in this process is used to form the high-energy molecules ATP (adenosine triphosphate) and NADH (reduced nicotinamide adenine ...
explains the palmitate synthesis- which is most common FA stored in Adipose tissue , elongation system and Desaturation system, compares oxidation with synthesis.
Beta-Oxidation may be defined as the oxidation of fatty acids on the beta-carbon atom.
This results in the sequential removal of a two carbon fragment, acetyl CoA.
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3. Definition
• Beta-Oxidation may be defined as the
oxidation of fatty acids on the beta-carbon
atom.
• This results in the sequential removal of a two
carbon fragment, acetyl CoA.
4. • Three stages
• Activation of fatty acids occurring in the
cytosol
• Transport of fatty acids into mitochondria
• Beta-Oxidation proper in the mitochondrial
matrix
• Fatty acids are oxidized by most of the
tissues in the body.
• Brain, erythrocytes and adrenal medulla
cannot utilize fatty acids for energy
requirement.
5. • Fatty acids are activated to acyl CoA by thiokinases or
acyl CoA synthetases
• The reaction occurs in two steps and requires ATP,
coenzyme A and Mg2+
• Fatty acid reacts with ATP to form acyladenylate which
then combines with coenzyme A to produce acyl CoA.
• Two high energy phosphates are utilized, since ATP is
converted to pyrophosphate (PPi).
• The enzyme inorganic pyrophosphafase hydrolyses
PPi to phosphate.
• The immediate elimination of PPi makes this reaction
totally irreversible.
7. • The inner mitochondrial membrane is
impermeable to fatty acids.
• A specialized carnitine carrier system
(carnitine shuttle) operates to transport
activated fatty acids from cytosol to the
mitochondria.
• This occurs in four steps
1. Acyl group of acyl CoA is transferred to
carnitine (β-hydroxy γ-trimethyl aminobutyrate)
8. catalyzed by carnitine acyltransferasIe (CAT)
(present on the outer surface of inner
mitochondrial membrane).
2. The acyl-carnitine is transported across the
membrane to mitochondrial matrix by a
specific carrier protein.
3. Carnitine acyl transferase ll (found on the
inner surface of inner mitochondrial
membrane) converts acyl-carnitine to acyl
CoA.
4. The carnitine released returns to cytosol for
reuse.
10. • Each cycle of β -oxidation, liberating a two
carbon unit-acetyl CoA, occurs in a
sequence of four reactions
1. Oxidation
2. Hydration
3. Oxidation
4. Cleavage
11. 1.Oxidation
• Acyl CoA undergoes dehydrogenation by an
FAD-dependent flavoenzyme, acyl CoA
dehydrogenase.
• A double bond is formed between α and β
carbons (i.e., 2 and 3 carbons)
2.Hydration:
• Enoyl CoA hydratase brings
• about the hydration of the double bond to
form β -hydroxyacyl CoA.
12. 3.Oxidation
• β-Hydroxyacyl CoA dehydrogenase
catalyses the second oxidation and generates
NADH.
• The product formed is β-ketoacyl CoA.
4.Cleavage
• The final reaction in β -oxidation is the
liberation of a 2 carbon fragment, acetyl CoA
from acyl CoA.
• This occurs by a thiolytic cleavage catalysed
by β-ketoacyl CoA thiolase (or thiolase).
13. • The new acyl CoA, containing two
carbons less than the original,
reenters the β-oxidation cycle.
• The process continues till the fatty acid
is completely oxidized.
14. β-Oxidation of fatty acids
O
R – CH2 – CH2 – CH2 – C – O
Fatty acid
ATP
Mg+2
ADP + PPi
CoASH
Thiokinase
O
R – CH2 – CH2 – CH2 – C –SCoA
Acyl CoA
Cytosol
Carnitine Transport system
Mitochondria
15. O
R – CH2 – CH2 – CH2 – C – SCoA
Acyl CoA
SIDS
FAD
2ATP ----- ETC FADH2
Acyl CoA
Dehydrogenase
O
R – CH2 – CH2
CH2 – C – SCoA
Trans-enoyl CoA
H2 O
Enoyl CoA
Hydratase
OH
O
R – CH2 – CH – CH2 – C – SCoA
β - Hydroxyacyl CoA
16. OH
O
R – CH2 – CH – CH2 – C – SCoA
β - Hydroxyacyl CoA
Acyl CoA
NAD
3ATP ----- ETC
NADH + H+
O
β-Hydroxy Acyl CoA
Dehydrogenase
O
R – CH2 – C – CH2 – C – SCoA
β - Ketoacyl CoA
Thiolase
O
R – CH2 – C – SCoA
Acyl CoA
O
CH3 – C – SCoA
Acetyl CoA
TCA
Cycle
17. Oxidation of palmitoyl CoA
• Palmitoyl CoA + 7 CoASH + 7 FAD +
7 NAD+ + 7 H2O
8 Acetyl CoA + 7
FADH2 + 7 NADH + 7H+
• Palmitoyl CoA undergoes 7 cycles of β -
oxidation to yield 8 acetyl CoA.
• Acetyl CoA can enter citric acid cycle and
get completely oxidized to CO2 and H2O.
18. Energetics of β -oxidation
Mechanism
I. β- 0xidation 7 cycles
7 FADH2 [Oxidized by electron transport Chain (ETC)
each FADH2 gives 2 ATP ]
7 NADH (Oxidized by ETC, each NADH
Liberate 3A TP)
ATP yield
14
21
II. From 8 Acetyl CoA
Oxidized by citric acid cycle, each acetyl CoA
provides 12 A TP
96
Total energy from one molecule of palmitoyl CoA
131
Energy utilized for activation
(Formation of palmitoyl Co A)
Net yield of oxidation of one molecule of palmitate
-2
=129
19. Sudden infant death syndrome (SIDS)
• Unexpected death of healthy infants, usually
overnight
• Due to deficiency of medium chain acyl CoA
dehydrogenase.
• Glucose is the principal source of energy, soon
after eating or feeding babies.
• After a few hours, the glucose level and its
utilization decrease and the rate of fatty acid
oxidation must simultaneously increase to meet
the energy needs.
• The sudden death in infants is due to a blockade
in β -oxidation caused by a deficiency in medium
chain acyl CoA dehydrogenase (MCAD)
20. Jamaican vomiting sickness
• This disease is characterized by severe
hypoglycemia, vomiting, convulsions, coma
and death.
• lt is caused by eating unriped ackee fruit
which contains an unusual toxic amino acid,
hypoglycin A.
• This inhibits the enzyme acyl CoA
dehydrogenase and thus β -oxidation of fatty
acids is blocked, leading to various
complications
21. • Abnormalities in transport of fatty acids into
mitochondria & defects in oxidation leads to
deficient energy production by oxidation of
long chain fatty acids.
• Features:
• Hypoketotic hypoglycemia,
hyperammonemia, skeletal muscle
weakness & liver diseases.
• Acyl carnitine accumulates when the
transferases or translocase is deficient.
• Dietary supplementation of carnitine
improve the condition.
22. • Oxidation of odd chain fatty acids is similar
to that of even chain fatty acids.
• At the end 3 carbon unit, propionyl CoA is
produced.
• Propionyl CoA is converted into succinyl
CoA.
• Succinyl CoA is an intermediate in TCA cycle
• So, propionyl CoA is gluconeogenic.
23. • Propionyl CoA is carboxylated to D-methyl
malonyl CoA by a biotin dependent
carboxylase.
• Biotin is B7 vitamin & ATP is utilized in this
step.
• Recemase:
• Recemase acts upon D-methyl malonyl CoA
to give L-methyl malonyl CoA.
• This reaction is essential for the entry of this
compound into metabolic reactions of body.
24. • Mutase:
• Mutase catalyzes the conversion of L-methyl
malonyl CoA (a branched chain compound)
to succinyl CoA (a straight chain
compound).
• Mutase is an vitamin B12 dependent enzyme.
• Succinyl CoA enters the TCA cycle, &
converted into oxaloacetate, it is used for
gluconeogenesis.
• Propionyl CoA is also derived from
metabolism of valine & isoleucine.
26. • Propionyl CoA carboxylase deficiency:
• Characterized by propionic acidemia,
ketoacidosis & developmental abnormalities.
• Methyl malonic aciduria:
• Two types of methyl malonic acidemias
• Due to deficiency of vitamin B12
• Due to defect in the enzyme methyl malonyl
CoA mutase or recemase.
• Accumulation of methyl malonic acid in the
body.
27. • Methyl malonic acid is excreted into urine.
• Symptoms:
• Severe metabolic acidosis, damages the
central nervous system & growth retardation.
• Fetal in early life.
• Treatment:
• Some patients respond to treatment with
pharmacological doses of B12.
28. • Oxidation of fatty acids on α-carbon atom is
known as α-oxidation.
• In this, removal of one carbon unit from the
carboxyl end.
• Energy is not produced.
• No need of fatty acid activation & coenzyme A
• Hydroxylation occurs at α-carbon atom.
• It is then oxidized to α-keto acid.
• This, keto acid undergoes decarboxylation,
yielding a molecule of CO2 & FA with one
carbon atom less.
29. • Occurs in endoplasmic reticulum.
• Some FA undergo α - oxidation in
peroxisomes.
• α- oxidation is mainly used for fatty acids that
have a methyl group at the beta-carbon,
which blocks beta- oxidation.
• Major dietary methylated fatty acid is
phytanic acid.
• It is derived from phytol present in
chlorophyll, milk & animal fats.
30. Refsum’s disease
• Due to deficiency of the enzyme α-hydroxylase
(phytanic acid oxidase)
• α – oxidation does not occur.
• Phytanic acid does not converted into compound
that can be degraded by beta –oxidation.
• Phytanic acid accumulates in tissues.
• Symptoms:
• Severe neurological symptoms, polyneuropathy,
retinitis pigmentosa, nerve deafness & cerebellar
ataxia.
• Restricted dietary intake of phytanic acid
(including milk-is a good source of phytanic acid)
31. Omega- oxidation
• Minor pathway, takes place in microsomes.
• Catalyzed by hydroxylase enzymes involving
NADPH & cytochrome P-450.
• Methyl (CH3) group is hydroxylated to CH2OH
& subsequently oxidized with the help of
NAD+ to COOH group to produce
dicarboxylic acids.
• When β-oxidation is defective & dicarboxylic
acids are excreted in urine causing
dicarboxylic aciduria.
