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1. LIPID METABOLISM

2. CONTENTS
 INTRODUCTION TO LIPIDS
 CLASSIFICATION OF LIPIDS
 FATTY ACIDS
 OXIDATION OF FATTY ACIDS
 PHOSPHOLIPIDS
 LIPID METABOLISM
 STEPS IN LIPID DIGESTION AND ABSORPTION
 LIPID STORAGE DISEASE
 KETONE BODIES
 CHOLESTEROL SYNTHESIS
 CONCLUSION
 REFERENCE

3. INTRODUCTION
Lipids may be defined as compounds which are relatively insoluble in water
but freely soluble in nonpolar organic solvents like benzene, chloroform,
ether, hot alcohol, acetone etc and it constitute a heterogeneous group of
compounds of biochemical importance.

4. FUNCTIONS OF LIPIDS
 Storage form of energy (triglycerides)
 Structural components of biomembranes (phospholipids and cholesterol)
 Metabolic regulators (steroid hormones and prostaglandins)
 Act as surfactants, detergents and emulsifying agents
 Act as electric insulators in neurons
 Provide insulation against changes in external temperature (subcutaneous fat)
 Give shape and contour to the body
 Protect internal organs by providing a cushioning effect (pads of fat)
 Help in absorption of fat soluble vitamins (A, D, E and K)
 Improve taste and palatability to food.

5. CLASSIFICATION OF LIPIDS
Based on the chemical nature, lipids are classified as
Simple lipids
Compound
lipids
Derived lipids
Lipids
complexed to
other compounds
(proteolipids and
lipoproteins)

6. SIMPLE LIPIDS
They are esters of fatty acids with glycerol or other higher alcohols. They are
subclassified as:
 Triacylglycerol
 Waxes
DERIVED LIPIDS
They are compounds which are derived from lipids or precursors of lipids e.g. fatty
acids, steroids, prostaglandins, leukotrienes

7. PHOSPHOLIPIDS CONTAINING
PHOSPHORIC ACID
NITROGEN CONTAINING GLYCEROPHOSPHATIDES:
 Lecithin
 Cephalin
 Phosphatidyl serine
NON-NITROGEN GLYCEROPHOSPHATIDES
 Phosphatidyl inositol
 Phosphatidy glycerol
 cardiolipin
PLASMALOGENS, HAVING LONG CHAIN ALCOHOL
 Choline plasmalogen
 Ethanolamine plasmalogen
PHOSPHO SPHINGOSIDES, WITH SPHINGOSINE
SPHINGOMYELIN.
NON-PHOSPHORYLATED LIPIDS
GLYCOSPHINGOLIPIDS (CARBOHYDRATE)
 Cerebrosides
 Globosides
 Ganglioside
SULFOLIPIDS OR SULFATIDES
 Sulfated cerebrosides
 Sulfated globosides
 Sulfated gangliosides
They are fatty acids esterified with alcohol but in addition they contain other groups .
Depending on these extra groups, they are subclassified as
COMPOUND LIPIDS

8. FATTY ACIDS
Fatty acids, are included in the group of derived lipids. It is the most common
component of lipids in the body. They are generally found in ester linkage in different
classes of lipids. In the human body, free fatty acids are formed only during
metabolism.

9. CLASSIFICATION OF FATTY ACIDS
Depending on total no. of carbon atoms
 Even chain - having carbon atoms 2,4,6
 Odd chain - having carbon atoms 3, 5, 7
Depending on length of hydrocarbon chain
 Short chain - 2 to 6 carbon atoms
 Medium chain - 8 to 14 carbon atoms
 Long chain - 16 and above, usually up to 24 carbon atoms.
Depending on nature of hydrocarbon chain
 Saturated fatty acids
 Unsaturated fatty acids

10. PROPERTIES OF FATTY ACIDS
1. Hydrogenation
Unsaturated fatty acids may be converted to the saturated fatty acids by hydrogenation of double bond.
2. Halogenation
When treated with halogens under mild conditions, the unsaturated fatty acids can take up two halogen atoms,
at each double bond to form the halogenated derivative of the fatty acid.
The number of halogen atoms taken up will depend on the number of double bonds

11. 3. Melting point
The short and medium chain fatty acids are liquids, whereas long chain fatty acids are solids at 25
degree celcius. The solubility in water decreases, while melting and boiling points increase, with
increase in chain length
4. Salt formation
Saturated and unsaturated fatty acids form salts with alkali.
Sodium and potassium salts of long chain fatty acids are called soaps. Calcium and magnesium soaps
are insoluble. Calcium soaps are used in grease.
5. Ester formation
Both saturated and unsaturated fatty acids form esters with alcohols, especially with glycerol. Fatty
acids can form mono-, di-or tri-esters with alcohol groups of glycerol. Triglycerides or triacylglycerols
are also known as neutral fat
Glycerol + fatty acid → Monoacylglycerol
Monoglyceride + fatty acid → Diacylglycerol
Diglyceride + fatty acid →Triglyceride or triacylglycerol

12. FATTY ACID SYNTHESIS
 Occurs mainly in liver and adipocytes , in mammary glands during lactation and also occurs in
cytoplasm
 When glucose is plentiful large amounts of acetyl CoA are produced by glycolysis and can be used
for fatty acid synthesis
Three stages of fatty acid synthesis
A. Transport of acetyl COA into cytosol
B. Carboxylation of acetyl coA
C. Assembly of fatty acid chain

13. DE NOVO SYNTHESIS OF FATTY ACIDS
 Fatty acid synthesis is the process of combining eight two carbon fragments to form 16
carbon saturated fatty acid palmitate
 Palmitate can then be modified to give rise to the other fatty acids these modifications may
include
 Chain elongation to give longer fatty acids such as 18 carbon stearate
 Desaturation giving unsaturated fatty acids

14. OXIDATION OF FATTY ACIDS
Fatty acids are an important source of energy
Oxidation is the process where energy is produced by degradation of fatty acids
There are two types of fatty acids oxidation
 Beta oxidation of fatty acids
 Alpha oxidation of fatty acids

15. BETA OXIDATION OF FATTY ACIDS
 Beta oxidation is the process by which fatty acids in the form of Acetyl –coA molecules
are broken down in mitochondria or in peroxisomes to generate Acetyl CoA to enter the
TCA cycle
 It occurs in many tissues including liver, kidney and heart
 Fatty acids oxidation doesnt occur in the brain as fatty acid cant be taken up by that
organ
It involves three stages
1. Activation of fatty acids in the cytosol
2. Transport of activated fatty acids into mitochondria
3. Beta oxidation proper in the mitochondrial matrix

16. BETA OXIDATION OF FATTY ACID WITH AN
ODD NUMBER OF CARBONS
Chains with an odd-number of carbons are oxidized in the same manner as even-numbered chains,
but the final products are propionyl CoA and acetyl CoA.
 Propionyl CoA is converted into succinyl CoA in a reaction that involves Vitamin B12.
 Succinyl CoA can then enter the citric acid cycle.
Animals cannot make glucose from even carbon fatty acids. The only scope for glucose synthesis
from fatty acids is from the propionyl CoA left behind after the beta-oxidation of odd carbon fatty
acids.

17. BETA OXIDATION OF UNSATURATED
FATTY ACIDS
 In the oxidation of unsaturated fatty acids most of the reactions are the same as those for saturated fatty
acids only two additional enzymes an isomerase and a reductase are needed to degrade a wide range of
unsaturated fatty acids
 Energy yield is less by the oxidation of unsaturated fatty acids since they are less reduced
 Per double bonds 2 ATP are less formed sine the first step of dehydrogenation to introduce double bond
is not required as the double bond already exists

18. CONTROL OF FATTY ACID
METABOLISM
Acetyl CoA carboxylase plays an essential role in regulating fatty acid synthesis and
degradation
The carboxylase is controlled by hormones
 Glucagon
 Epinephrine
 Insulin
Another regulatory factors
 Citrate
 Palmitoyl CoA and
 AMP

19. SIGNIFICANCE OF FATTY ACID
METABOLISM
Fatty acids are taken up by cells where they may serve as
 precursors in the synthesis of other compounds
 as fuels for energy production
 as substrates for ketone body synthesis
Ketone bodies may then be exported to other tissues where they can be used for energy production
. In addition some cells synthesize fatty acids for storage or export

20. INTERMEDIATES IN SYNTHETIC PROCESSES
Fatty acids are intermediates in the synthesis of other important compounds include
phospholipids , Eicosanoids including prostaglandins and leucotrienes which play a role in
physiological regulation
ENERGY
 Fats are an important source of dietary calories
 Typically 30-40% of calories in the American diet are from fat
 Fat is the major form of energy storage

21. FATE OF ABSORBED FAT
 The absorbed triglycerides are transported in blood as chylomicrons. Which
are taken up by adipose tissue and liver.
 Liver synthesises endogenous triglycerides. These are transported as VLDL
and are deposited in adipose tissue.
 Triglycerides in adipose tissue are lysed to produce free fatty acids
 Free fatty acids are taken up by the cells, and are then oxidized to get
energy.

22. ROLE OF FATS IN GASTRIC EMPTYING
 Fats delay the rate of emptying of stomach
 Action is brought about by secretion of enterogastrone
 Enterogastrone inhibits gastric motility and retards the discharge of bolus of food from the
stomach
 Thus fats have a high satiety value

23. ESSENTIAL FATTY ACIDS
 Linoleic acid and linolenic acid are the only fatty acids which cannot be
synthesized in the body. They have to be provided in the food hence they are
essential fatty acids.
 Arachidonic acid can be formed, if the dietary supply of linoleic acid is sufficient.
Normal dietary allowance of PUFA is 2–3% of total calories. Deficiency causes
acanthosis, hyperkeratosis and hypercholesterolemia.

24. PHOSPHOLIPIDS
They contain glycerol, fatty acids and a nitrogenous base. Synthesized in smooth endoplasmic reticulum
and transferred to golgi apparatus
All cells except mature erythrocytes can synthesize phospholipids
Types
 Glycerophospholipids
 sphingophospholipids

25. ACTION OF DIFFERENT
PHOSPHOLIPASES
Phospholipases A1
 Found in many mammalian tissues
 Removes fatty acid from C1
Phospholipases A2
 Found in many tissues and pancreatic juice
 When acts on phospholipids releases arachidonic acid
 Inhibited by glucocorticoids

26. PHOSPHOLIPASE C
 Cleaves phosphate group at C3
 Found in liver lysosomes and some bacteria
 Role in producing secondary messenger
PHOSPHOLIPASE D
 Found primarily in plant tissues
 Removes the compound with alcohol group on C3

27. LIPOGENESIS
 Lipogenesis is the process your body uses to convert carbohydrates into fatty acids
which are the building blocks of fats
 Fat is an efficient way for your body to store energy

28. LIPOLYSIS
 The breakdown of lipids and involves hydrolysis of triglycerides into glycerol and free
fatty acids
 Predominantly occurring in adipose tissue , lipolysis is used to mobilize stored energy
during fasting or exercise

29. LIPID METABOLISM
Referred to the synthesis and degradation of lipids within the cells either breakdown or
storage of fats for energy
These fats are obtained from consuming food and absorbing them or they are synthesized
by an animals liver

30. CENTRE OF LIPID METABOLISM
Acetyl CoA is at the center of lipid metabolism it is produced from Fatty acids , glucose ,
amino acids , ketone bodies.
It produces energy generated by the complete oxidation of acetyl CoA to carbon di oxide
and water through the tricarboxylic acid cycle and oxidative phosphorylation
It can be converted to fatty acids which in turn give rise to
 Triglycerides
 Phospholipids
 Eicosanoids
 Ketone bodies
 Steroid hormones
 Bile acids

31. STEPS OF LIPID DIGESTION AND
ABSORPTION
STEP LOCATION ENZYMES
1 . Minor digestion Mouth and stomach Lingual / gastric lipase
2 . Major digestion Lumen of small intestines Pancreatic lipase , cholesterolterase
, phospholipase A2
3 . Formation of mixed micelles (
uses bile salts as biological
detergent)
Lumen of the small intestines
4 . Passive absorption of lipolytic
products
Into intestinal epithelial cells
5 . Assembly and export of
chylomicrons
From intestinal cells to the
lymphatics

32. DIGESTION OF LIPIDS
The major dietary lipids are triacyl glycerol, cholesterol and phospholipids. The average normal
Indian diet contains about 20–30 g of lipids per day.
Digestion in Stomach
Digestion in stomach occurs with the help of lingual lipase and gastric lipase. Lingual lipase is
more significant in newborn infants.
Digestion in Intestines
Emulsification occurs in digestion of lipids. The lipids are dispersed into smaller droplets; surface
tension is reduced; and surface area of droplets is increased

33. Bile Salts are important for digestion of lipids
The bile salts present in the bile lower surface tension. They emulsify the fat
intestine. The emulsification increases the surface area of the particles for
enzymes
Lipolytic Enzymes in intestines
Pancreatic lipase with colipase will further hydrolyse the neutral fats. The bile (pH 7.7)
duodenum serves to neutralize the acid chyme from the stomach and provides a pH
of pancreatic enzymes.

34. Digestion of Triglycerides
Digestion occurs with the help of pancreatic lipase, isomerase and colipase. The major end
the digestion of TAG are 2-MAG, 1-MAG, glycerol and fatty acids . Thus digestion of TAG
(incomplete)

35. Lingual lipase
Gastric lipase
Pancreatic triglyceride
lipase
Carboxyl ester lipase
Von ebners glands
Fundic gastric chief
cells
Pancreatic acinar cells
Pancreatic acinar cells
Hydrolysis of TG present in
food. Perception of fat taste
Hydrolysis of TG from food
Hydrolysis of TG from food
Hydrolysis of TG,
phospholipids ,
lysophospholipids and
ceramides

36. SIGNIFICANCE OF LINGUALAND GASTRIC
LIPASES
 Plays important role in lipid digestion in neonates since milk is the main source of energy
 Important digestive enzymes in pancreatic insufficiency such as cystic fibrosis or other pancreatic disorders
 Lingual and gastric lipases can degrade triglycerides with short and medium chain fatty acids in patients
with pancreatic disorders despite near or complete absence of pancreatic lipase

37. CONTROL OF LIPID DIGESTION
HORMONAL CONTROL
CHOLECYSTOKININ
Site of release – released in blood from jejunum and lower duodenum and in response to lipids
and partially digested proteins entering small intestines
Actions
Gall bladder – contraction and release of bile
Pancreatic exocrine cells – release of digestive enzymes
Decreases gastric motility
SECRETIN
Site –released in blood from other intestinal cells in response to low PH of chyme
Actions - Release of watery solution by pancreas and liver , high in bicarbonate , Appropriate pH
for action of pancreatic enzymes

38. LIPID ABSORPTION AND TRANSPORT
Fatty acids and monoglycerides are
emulsified by bile salts to form micelles
Fatty acids enter the epithelial cells and
link to form triglycerides
Triglycerides combine with proteins
inside the golgi body to form
chylomicrons
Chylomicrons enter the lacteal and are
transported away from the intestine

39. TRANSPORT OF LIPIDS BY LIPOPROTEINS
Four classes of lipoproteins are chylomicrons , very low density lipoproteins, low density lipoproteins ,
high density lipoproteins
 Chylomicrons : form in small intestinal mucosal cells and contain exogenous lipids . They enter villi
lacteals are carried into the systemic circulation into adipose tissue where their triglyceride fatty acids
are released and stored in the adipocytes and used by mucosal cells for ATP production

40.  VLDL contain endogenous triglycerides . They are transport vehicle that carry
triglycerides synthesized in hepatocytes to adipocytes for storage VLDLs are converted to
LDLs
 HDL remove excess cholesterol from body cells and transport it to the liver for elimination
 LDL carry about 75% of total blood cholesterol and deliver it to cells throughout the body .
When present in excessive numbers LDLs deposit cholesterol in and around smooth
muscle fibers in arteries

41. LIPID PROFILE (RFERENCE RANGE)
Total serum cholesterol : 140- 200 mg/dl
Serum LDL cholesterol – less than 100mg/dl
Serum triglycerides : 50- 150 mg/dl
Serum HDL cholesterol : 40 – 70mg/dl
 HDL less than 40 mg/dl in men and less than 50mg/dl in women increases the risk of heart
disease
 HDL more than 60mg/dl decreases the risk of heart disease
 LDL/HDL ratio – less than 3 is cardio protective and more than 5 increases the risk
 Total cholesterol/HDL ratio should be less than 5:1 . Ideal is 3.5:1

42. ABNORMALITIES IN ABSORPTION OF LIPIDS
 Defective digestion : Daily excretion of fat in feces is more than 6 g per day It is due
to chronic diseases of pancreas. In such cases, unsplit fat is seen in feces.
 Defective absorption: if the absorption alone is defective, most of the fat in feces may
be split fat, i.e. fatty acids and monoglycerides. Defective absorption may be due to
obstruction of bile duct , gallstones, tumors of head of pancreas, enlarged lymph
glands, etc
 Chyluria. There is an abnormal connection between the urinary tract and lymphatic
drainage system of the intestine. Urine appears milky due to lipid droplets.

43. LIPOTROPIC FACTORS
 They are required for the normal mobilization of fat from liver. Therefore
deficiency of these factors can result in fatty liver.
 Choline: Feeding of choline has been able to reverse fatty changes in
animals
 Lecithin and Methionine- They help in synthesis of apoprotein and choline
formation
 Vitamin E and selenium give protection due to their anti-oxidant effect.
 Omega 3 fatty acids present in oils have a protective effect against fatty
liver

44. LIPID STORAGE DISEASES OR SPHINGOLIPIDOSES
 They form a group of lysosomal storage disease . The diseases result from failure of
breakdown of a particular sphingolipid due to deficiency of a single enzyme.
 The children affected by these diseases are severely mentally retarded. Diseases include
Niemann Picks disease, Gauchers disease and Tay-Sachs disease.
 Mental retardation, neurological deficit and skeletal abnormalities are common presenting
symptoms

45. HYPERLIPIDEMIAS
 The elevation of lipids in plasma leads to the deposition of cholesterol on the arterial walls, leading to
atherosclerosis . The coronary and cerebral vessels are more commonly affected.
 Thromboembolic episodes in these vessels lead to ischemic heart disease and cerebrovascular accidents.
 The deposition of lipids in subcutaneous tissue leads to xanthomas.
 Xanthelasma are lipid deposits under the periorbital skin contains cholesterol
 Deposits of lipids in cornea lead to corneal arcus indicating hypercholesterolemia.

46. CLINICAL APPLICATIONS
 Excessive fat deposits cause obesity. Truncal obesity is a risk factor for
heart attack.
 Abnormality in cholesterol and lipoprotein metabolism leads to
atherosclerosis and cardiovascular diseases
 In diabetes mellitus, the metabolisms of fatty acids and lipoproteins are
deranged, leading to ketosis

47. KETONE BODIES
 Ketone bodies are water soluble compounds that are produced as by products
when fatty acids are broken down for energy in the liver and kidney.
 They are used as a source of energy in the heart and brain. In the brain, they are
a vital source of energy during fasting.
 The three endogenous ketone bodies are acetone, acetoacetic acid, and beta-
hydroxybutyric acid
 They are transported from liver to other tissues, where acetoacetate and beta-
hydroxybutyrate can be reconverted to acetyl-CoA to produce energy in the
mitochondrial matrix

48. KETOGENESIS
Ketogenesis is the process by which ketone bodies are produced as a result of fatty acid
breakdown.
Ketone bodies are produced mainly in the mitochondria of liver cells. Its synthesis
occurs in response to low glucose levels in the blood.
The three ketone bodies are:
 Acetoacetate
 Acetone
 β-hydroxybutyrate

49.  Regulation: Ketogenesis may or may not occur, depending on levels of available carbohydrates
in the cell or body.
 When the body has no free carbohydrates available, fat must be broken down into acetyl-CoA in
order to get energy.
 Both acetoacetate and beta-hydroxybutyrate are acidic, and, if levels of these ketone bodies are
too high, the pH of the blood drops, resulting in ketoacidosis.
 Ketoacidosis is known to occur in untreated Type I diabetes and in alcoholics without intake of
sufficient carbohydrates

50. KETOACIDOSIS
 Is a metabolic state associated with high concentrations of ketone bodies,
formed by the breakdown of fatty acids and the deamination of amino acids. The
two common ketones produced in humans are acetoacetic acid and β-
hydroxybutyrate.
 Ketoacidosis occurs when the body is producing large quantities of ketone
bodies via the metabolism of fatty acids (ketosis) and the body is producing
insufficient insulin to slow this production.

51. There are two common types of Ketoacidosis i.e. diabetic and alcoholic ketoacidosis.
 In diabetic patients, ketoacidosis is usually accompanied by insulin deficiency, hyperglycemia,
and dehydration. Particularly in type 1 diabetics the lack of insulin in the bloodstream prevents
glucose absorption and can cause ketone body production
 In alcoholic ketoacidosis, alcohol causes dehydration and blocks the first step of gluconeogenesis.
The body is unable to synthesize enough glucose to meet its needs, thus creating an energy crisis
resulting in fatty acid metabolism, and ketone body formation

52. KETONURIA
Ketonuria is a medical condition in which ketone bodies are present in the urine. It is seen in conditions in which the
body produces excess ketones as an alternative source of energy. It is seen during starvation or more commonly in
type I diabetes mellitus.
Causes of ketonuria
 Metabolic abnormalities such as diabetes, renal glycosuria, or glycogen storage disease
 Dietary conditions such as starvation, fasting, high protein, or low carbohydrate diets, prolonged vomiting, and
anorexia
 Conditions in which metabolism is increased such as hyperthyroidism, fever, pregnancy or lactation
 In nondiabetic persons, ketonuria may occur during acute illness or severe stress. Approximately 15% of
hospitalized patients may have ketonuria, even though they do not have diabetes.
 In the nondiabetic patient, ketonuria reflects a reduced carbohydrate metabolism and an increased fat
metabolism.

53. CHOLESTEROL SYNTHESIS,TRANSPORT &
EXCRETION
 Cholesterol is present in tissues and in plasma either as free cholesterol or as a storage
form
 It is synthesized in many tissues from acetyl-CoA and is the precursor of all other
steroids in the body such as corticosteroids, sex hormones, bile acids, and vitamin D.
 Plasma low-density lipoprotein is the vehicle of uptake of cholesterol and cholesteryl
ester into many tissues.
 Free cholesterol is removed from tissues by plasma high-density lipoprotein (HDL) and
transported to the liver, where it is eliminated from the body either unchanged or after
conversion to bile acids in the process known as reverse cholesterol transport.

54.  Cholesterol is a major constituent of gallstones. However, its chief role in pathologic processes is
as a factor in the genesis of atherosclerosis of vital arteries, causing cerebrovascular, coronary and
peripheral vascular disease.
 Biosynthesis of cholesterol: Cholesterol synthesis occurs in the cytoplasm and microsomes from
the two-carbon acetate group of acetyl-CoA.
 Biosynthesis of cholesterol in the liver accounts for approximately 10%, and in the intestines
approximately 15%, of the amount produced each day

55. ATHEROSCLEROSIS
 Atherosclerosis is a disease in which plaque builds up on the insides of arteries.
 It is a syndrome affecting arterial blood vessels caused by low density and high
density lipoproteins
The atheromatous plaque is divided into three distinct components:
1. The atheroma which is the nodular accumulation at the center of large plaques
2. Underlying areas of cholesterol crystals
3. Calcification at the outer base of older/more advanced lesions.

56. Atherosclerosis can affect any artery in the body, including arteries in the heart, brain,
arms, legs, and pelvis.
Symptoms of Atherosclerosis
 Restriction of blood flow to the heart muscle due to atherosclerosis can cause angina
pectoris or a myocardial infarction
 Restriction of blood flow to the muscles of the legs causes intermittent claudication
(pains in the legs brought about by walking and relieved by rest).
 Narrowing of the arteries supplying blood to the brain may cause transient ischemic
attacks and episodes of dizziness

57. Treatment
 Anticoagulant drugs have been used to minimize secondary clotting and embolus
formation.
 Vasodilator drugs are helpful in providing symptom relief
 Balloon angioplasty can open up narrowed vessels and promote an improved blood
supply.
 The blood supply to the heart can also be restored by coronary artery bypass surgery.

58. FATTY LIVER
 It is also known as fatty liver disease (FLD), is a reversible condition where large vacuoles of triglyceride
fat accumulate in liver cells via the process of steatosis (i.e. abnormal retention of lipids within a cell).
 Causes: Fatty liver is commonly associated with alcohol or metabolic syndrome (diabetes, hypertension,
obesity and dyslipidemia)
 Diagnosis of Fatty Liver: in routine blood screening or images of the liver obtained by an ultrasound test,
CT scan, or MRI may suggest the presence of a fatty liver or liver biopsy

59. Treatment of fatty liver
 simple fatty liver may not require treatment.
 Reducing or eliminating alcohol use can improve fatty liver due to alcohol toxicity.
 Controlling blood sugar may reduce the severity of fatty liver in patients with diabetes

60. HYPERCHOLESTEROLEMIA
 Hypercholesterolemia is a condition in which there is too much cholesterol in the body.
 High cholesterol raises risk for heart disease, heart attack, and stroke. When there is too much
cholesterol circulating in the blood, it can create sticky deposits (called plaque) which
completely block blood flow through an artery, causing heart attack or stroke.
 There are two types of cholesterol -- HDL (high-density lipoproteins, or "good" cholesterol)
and LDL (low-density lipoproteins, or "bad" cholesterol). There is a third kind of fatty
material, triglycerides, found in the blood

61.  The most important risk factors for high cholesterol are: Being overweight or obese, Eating a
diet high in saturated fat. Not getting enough exercise, Family history of heart disease, High
blood pressure, Smoking, Diabetes etc
 Treatment Approach: Lowering your cholesterol level reduces your risk of heart disease and
stroke. Changes in lifestyle -- better diet, more exercise and specific cholesterol-lowering
medications are often prescribed
Total cholesterol levels (mg/dL):
 Desirable: Below 200
 Borderline high: 200 - 239
 High: Above 240

62. CONCLUSION
Lipid metabolism is very complex and is regulated by a complex signaling
network in cells . The same lipid molecule via different signaling pathways or
under different conditions can generate different metabolites and helps in storage
of energy

63. REFERENCE
 TEXTBOOK OF BIOCHEMISTRY – DM VASUDEVAN
 TEXTBOOK OF BIOCHEMISTRY – SATHYANARAYANAN
 ARTICLES OF MEDICAL BIOCHEMISTRY – SUMANTA MONDAL
 ARTICLES OF LIPID METABOLISM AND DISEASE – QUI QUN TANG