lipid metabolism

1. LIPID METABOLISM

2. • Lipids are important for cell structure and
function.
Triacylglycerols —the body fuel reserve
Lipids constitute about 15-20% of the body
weight in humans. In this 85 -90% is TAG.
INTRODUCTION

4. Why should fat be the fuel reserve of the body?
1. Triacylglycerols (TG) are highly concentrated
form of energy, yielding 9 Cal/g.
2. The triacylglycerols are non-polar and hydrophobic in
nature, hence stored in pure form without any association
with water. One gram of glycogen combines with 2 g of
water for storage.

13. Triacylglycerol /fatty acid cycle
This process of lipolysis of TG and resterification of
FFA to TG is termed as triacylglycerol/fatty acid cycle.

22. TRIACYLGLYCEROL HYDROLYSIS

24. Fate of glycerol
The adipose tissue lacks the enzyme glycerol kinase,
So It is transported to liver where it is activated to glycerol 3-
phosphate.
It used for the synthesis of triacylglycerols and
phospholipids. Glycerol 3-phosphate may also enter
glycolysis by getting converted to dihydroxyacetone
phosphate.
Fate of free fatty acids
The fatty acids released in the adipocytes enter the
circulation and are transported in a bound form to albumin.
Some cannot oxidize fatty acids, e.g. brain, erythrocytes.

30. carnitine carrier system (carnitine shuttle)

33. - OXIDATION
- OXIDATION

73. Regulation of fatty acid synthesis
controlled by enzymes, metabolites, end products, hormones
and diet.
Acetyl CoA carboxylase
Acetyl CoA carboxylase exists as an inactive protomer
(monomer) or an active polymer. Citrate promotes polymer
formation.
palmitoyl CoA and malonyl CoA cause depolymerization of
the enzyme and, inhibit fatty acid synthesis.
Hormonal influence
Glucagon, epinephrine and norepinephrine inactivate the
enzyme by cAMPdependent phosphorylation.
Insulin, on the other hand, dephosphorylates and activates
the enzyme.

74. Dietary regulation :
Consumption of high carbohydrate or fat-free diet increases the
synthesis of acetyl CoA carboxylase and fatty acid synthase, which
promote fatty acid formation. On the other hand, fasting or high
fat diet decreases fatty acid production by reducing the synthesis
of these two enzymes.
Availability of NADPH :
The reducing equivalents for fatty acid synthesis are provided by
NADPH which come either from citrate (acetyl CoA) transport or
hexose monophosphate shunt.
About 50-60% of required NADPH is obtained from HMP shunt,
which significantly influences fatty acid synthesis.

108. Phospholipase A2 hydrolyses the fatty acid at C2
position of phospholipids. Phospholipase A2 acts on
phosphatidyl inositol to liberate arachidonic acid, the
substrate for the synthesis of prostaglandins
phospholipase B to remove the second acyl group
at C2 position.
Phospholipase A1 specifically cleaves the fatty
acid at C1 position resulting in lysophospholipid.
Phospholipase C specifically cleaves the bond
between phosphate and glycerol of phospholipids.
This enzyme is present in lysosomes of hepatocytes.
Phospholipase D hydrolyses and removes the
nitrogenous base from phospholipids.

110. Role of LCAT in lecithin metabolism
Lecithin-cholesterol acyltransferase (LCAT) is a
plasma enzyme, synthesized in the liver.
This reaction is responsible for the reverse
cholesterol transport mediated by HDL