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roperties of Triacylglycerols

1. Hydrolysis
x triacylglycerols undergo stepwise enzymatic
hydrolysis to finally liberate 2 free FA and
x catalyzed by lipases
x important for digestion of fat in the GIT and fat
mobilization from the adipose tissues
0. Saponification
x hydrolysis by alkali to produce glycerol and
Triacylglycerol + 3 NaOH 2 Glycerol + 3R-CooNa (soaps)
3. Rancidity
x term used to represent the deterioration of fats
and oils resulting in an unpleasant taste
x fats with UFA - more susceptible
x occurs when fats are exposed to air, moisture,
light and bacteria
Detabolism of Lipids

Cholesterol, the most feared among the lipids,

³Consumed through diet and produced in the
articipate in innumerable cellular functions;
Implicated in several health complications;
And blamed I am, for no fault of mine!´

x Best known steroid because of its association

with atherosclerosis
x biochemically of significance because it is the
precursor of a large # of equally important
1. Sex hormones 5. Cardiac glycosides
0. Bile acids 6. Sterols
3. Vit. D 7. Sitosterol
4. Adrenal cortical hormones 8. Alkaloids
Cholesterol in erspective

Cholesterol has many roles in health and

disease, both in its own right, and as a
precursor of a variety of biologically, important
Gallstone plaque

Acetate2 2 2 Cholesterol Dembranes

U V light
Vit. D Hormones
Bile Acids
Adrenal / gonads

x Cholesterol penetrates into the T. interna,

narrowing the vessels 2 decreasing blood
supply 2 causing D I
x cholesterol must be packaged as part of a
LIOROTEIN in order to be transported in
x its insolubility makes deposit troublesome
especially in atherosclerotic plaques and
x A high level of blood cholesterol, especially
that contained in LDL is a risk in
atherosclerotic ù disease, much attention is
being given to factors that lower cholesterol
 substitute vegetable products for meat and
dairy products
 consume more olyunsaturated fatty acids
that saturated products
 has a cholesterol lowering effects
b) Exercise
  HDL / LDL ratio which correlates negatively
with Atherosclerosis

'etone bodies acetoacetate

acetone TRUE ketones


ë-hydroxybutyrate-does not possess a keto

(C=0) group
'etone bodies 2 are water soluble and energy
liver - synthesis occur
mitochondrial matrix - where enzymes for
ketone bodies synthesis are located
oxidation of FA Acetyl CoA
some AA precursor for ketone
Reactions of 'etogenesis

1. Two moles of acetyl CoA condense to form

acetoacyl CoA
x reaction catalyzed by Thiolase (an enzyme
involved in the final step of ë-oxidation)
x hence acetoacetate synthesis is regarded as
the reversal of thiolase reaction of fatty acid
0. Acetoacyl CoA combines with another
molecule of acetyl CoA to produce ë-methyl
glutaryl CoA (HDC CoA)
x HDG CoA synthase, catalyzing the reaction,
regulates the synthesis of ketone bodies

3. HDG CoA lyase cleaves HDG CoA to produce

acetoacetate and acetyl CoA
4. Acetoacetate can undergo spontaneous
decarboxylation to form acetone

5. Acetoacetate can be reduced by a

dehydrogenase to ë-hydroxybutyrate

The C skeletons of some AA (ketogenic,

leucine, lysine, phenylalanine, etc.) is degraded
to acetoacetate or acyl CoA and to ketone
Energy yield from oxidation of ketone

1. Conversion of ë-hydroxybutyrate to
acetoacetate yields an NADH molecule, yields 3
AT molecules (by electron transport and
oxidative phosphorylation)

0. Each mole of acetyl CoA that is formed yields

10 moles of AT (via citric acid cycle, electron
transport, and oxidative phosphorylation)
3. The activation reactions require 1 mole of AT.

4. Therefore, oxidation of acetoacetate yields 04

moles (from 0 moles of acetyl CoA) - 1 mole
AT (expended during activation) = 03 moles of AT
oxidation of ë-hydroxybutyrate yields
3 moles of AT (from one NADH molecule) + 04
moles of AT (from 0 moles of acetyl CoA) -
mole of AT = 06 modes of AT
During prolonged starvation 2 ketone bodies are
the major fuel source for the brain and other parts
of the CNS

x Ability of the brain to utilize FA for energy is

x ketone bodies can meet 50-70% of the brain¶s
energy needs
In No individuals 2 constant production of
ketone bodies (liver)
 concentration in the blood 2 1 mg/dL
 excretion in urine is very low and
undetectable by routine tests (Rothera¶s test)
'etonemia 2 rate of synthesis of ketone bodies
exceeds the rate of utilization, their concentration
in the blood 

'etonuria 2 follows ketonemia, secretion of

ketone bodies in the urine
'etonemia ketosis (overall picture)
(+) acetone breath associated
with starvation and severe
uncontrolled DD
Glucagon 2 stimulates ketogenesis
Insulin 2 inhibits
'etogenic substances (promote ketone body
1. Fatty acids
0. Amino acids (leucine, lysine, tyrosine)

Antiketogenic substances (inhibits ketone body

1. Glucose
0. Glycerol
3. Glucogenic AA (glycine, alanine, serine,
Acetoacetate strong acids - when in 
ë-hydroxybutyrate concentration in the blood

Diabetic acidosis 2 dangerous 2 coma 2 death

if untreated
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