METABOLISM OF

ADIPOSE TISSUE
 Role of Adipose Tissue in Lipid
Metabolism
■ Adipose tissues carry all metabolic process of
any active tissues.
■ Calories are stored in it as triglycerides.
■ The triglycerides of adipose tissue are
continually undergoing hydrolysis (Lipolysis)
and re esterification.
 Role of Adipose Tissue in Lipid
Metabolism
■ The resultant of these two processes
determines the amount of FFA released
from adipose tissue into blood.
■ The glycerol liberated from the hydrolysis
can not be utilized by fat cell due to
deficiency of glycerol kinase enzyme so it
passes to blood.
■ FFA= Free fatty acids
■ Kinase is an enzyme that catalyzes the transfer
of phosphate groups from high-energy,
phosphate-donating molecules to specific
substrates. This process is known as
phosphorylation, where the substrate gains a
phosphate group and the high-energy ATP
molecule donates a phosphate group.
■ Thus insulin and a diet rich in
carbohydrates help the re esterification of
FAA and decrease their release into the
blood by increasing the uptake and
oxidation of glucose by adipose tissue.
■ Fasting glucagon, adrenaline
glucocorticoids and growth hormone have
the opposite effect.
 Metabolism of adipose tissue
■ The hydrolysis of triacylglycerol (lipolysis) is
under the control of the enzyme “hormone-
sensitive triacylglycerol lipase”.
■ This enzyme may exist in one of two forms: An
active form ”lipase a” which is phosphorylated,
and an inactive form “lipase b” which is
dephosphorylated.
■ Phosphorylation refers to an addition of a
phosphate group to a phosphate-accepting
amino acid, such as Serine and Tyrosine. A
phosphate group added onto a molecule
(usually a protein that is an enzyme) activates
it or, in some cases, deactivates it.
■ When this phosphate group “falls off,” or is
removed, once the protein has performed its
function and needs to be deactivated (in the
case of phosphorylation-based activation).
This is referred to as dephosphorylation.
FATTY LIVER AND
LIPOTROPIC
FACTOR
 FATTY LIVER
■ Fatty liver is an abnormal condition
characterized by increasing deposition of
lipids, mainly T.G. in the liver cells.
■ When accumulation of lipid becomes chronic,
fibrotic changes occur in the cells, which
progress to cirrhosis and impaired liver
function.
 FATTY LIVER

■ Normal fat content of the liver is about 5%

of its weight and is mainly phospholipids
but in fatty liver it may reach 20-30% and
is mainly in the form of neutral fat.
 Causes of fatty liver
1. Increased fat in diet, increased uptake of fats by
liver if this exceeds the capacity of the liver to
synthesis VLDL → fatty liver.
2. Over feeding carbohydrate (COH) → overload the
capacity of the liver to store it as glycogen →
converts CHO to TG, if this exceed the capacity of
the liver to synthesize VLDL → fatty liver.
3.Decreased oxidation of FA directs fatty acids to esterification
(TG). This decreases fatty acid oxidation occurs in the following
condition.
i. Deficiency of pantothenic acid .
ii. Deficiency of carnitine (choline deficiency).
iii. Alcoholism, alcoholic fatty liver is caused by:

A. Decreased FA oxidation as a result of oxidation of ethanol

to acetaldehyde leading to ↑ NADH/NAD ratio.
B. Increased fatty acid synthesis.
■ 4. Increased mobilization of fat from adipose tissue to liver
cell. This occurs in conditions characterized by decrease
carbohydrate utilization e.g. D.M., starvation. 5. Decreased
mobilization of fat from liver to blood. TG synthesized in the
liver are normally mobilized to blood by VLDL. Failure to
synthesize VLDL may be caused by decreased protein
synthesis (apolipoprotein), failure in conjugation or failure in
secretory mechanism. Decreased mobilization associated
with deficiency of lipotropic factors.
■ 6. Liver poisons e.g. chloroform puromycin and carbon
tetrachloride → decreased protein synthesis.
 Lipotropic Factors
■ These are substances that protect against and cure
fatty liver.
■ They include mainly the substances essential for
phospholipids synthesis.
■ Phospholipids are easily mobilized from liver and
less liable to deposition in liver cell.
These substances are:
■ 1. Choline → olecithin, choline plasmalogen,
sphingomyleine.
■ 2. Methionine → required for choline synthesis.
■ 3. Folic acid and B12 → transfer of CH3 group
(transmethylation).
■ 4. Inositol → phosphatidyl inositol.
KETONE BODY
METABOLISM
 Ketogenesis is a metabolic pathway that
produces ketone bodies, which provide an
alternative form of energy for the body.
 The body is constantly producing small
amounts of ketone bodies that can make 22
ATP each in normal circumstances, and it is
regulated mainly by insulin.
 In a state of ketosis, ketone body production is
increased when there are decreased
carbohydrates or increased fatty acids.
However, ketoacidosis can occur if too many
ketone bodies accumulate, such as in cases
uncontrolled diabetes.
 Ketogenesis produces acetone, acetoacetate, and
beta-hydroxybutyrate molecules by breaking down fatty
acids.
 These ketones are water-soluble lipid molecules made
up of two R-groups attached to a carbonyl group (C =
O). Because they are water soluble, they do not require
lipoproteins for transport. Of the three, acetoacetate
and beta-hydroxybutyrate are acidic, having pKa values
of 3.6 and 4.7 respectively.
FUNCTION
■ In healthy humans, the body is continually
making a small amount of ketones to be used
by the body for energy. In times of fasting,
even overnight while sleeping, the amount of
ketone bodies in the blood increases.