• One or more atoms of carbon are covalently linked to

other elements (hydrogen, oxygen, nitrogen).

• Organic compound
Lipids • Also known as fats
• Stores excess calories in the body
Examples of Organic Compounds • Carbohydrates, proteins and lipids
• Excess glucose in the blood will be transported here in
the form of triglycerides.
Adipose Cells • Fats are stored here.
Phospholipid Bilayer Most abundant in the cell membrane
• Linear chain of C-H bonds that terminate with
carboxylic acid group.
Type of Lipid: Fatty Acids • Good sources of energy
Plasma • Found in the blood, exist as free fatty acids.
• Composed of 90% water.
Albumin Free fatty acids bind here

FADH2 and NADH Products of the Krebs Cycle

Type of Lipid: Triglycerides
Short chain
• Have a glycerol backbone and three fatty acids.
• Attached to carbon atoms via ester bonds.
• Neutral lipids
• Good energy source
• Hydrophobic
• 80% of fats in the diet
• Large but light
4-6 carbons

Medium chain 8-12 carbons

Long chain More than 12 carbons

Saturated No double bond

Monounsaturated One double bond

Polyunsaturated More than one double bonds

Unsaturated Can add more hydrogen atoms

Cis forms • If the hydrogen atoms near double bonds are on the
same side of the chain. (Bends).
• Found in natural food.
If the hydrogen atoms are on the opposite side of the
chain. (Does not cause bending).
Trans forms • Increases LDL (bad cholesterol levels) in the blood.
Causes heart attack and stroke.
Hydrogenation • Conversion of cis to trans form.
• Liquid oil to solid fats - margarine
Saturated Fat Solid at room temperature. Mostly in animal food.

Unsaturated Fat • Plant oils

• Amphipathic with 4 fused hydrophobic rings called
perhydrocyclopentanophenanthrene rings
Type of Lipid: Cholesterol • A type of sterol that is produced/synthesized by
animals and humans (ergosterol in fungi)
• Endocrine glands  Steroid hormones
• Amphipathic
• Hydrophilic phosphate-containing groups
Type of Lipid: Phospholipids • Hydrophobic fatty-acid tails
• Glycerol backbone, 2 fatty acids and one phosphate
group
• Testosterone
• Aldosterone
Steroid Hormones • Cortisol
• Androgens
• Estrogen and Progesterone
• Hydrophobic, 4 fused rings
• Cholesterol esterified with fatty acid
Cholesteryl Ester • Good source of energy
Lipoprotein • Water soluble
Components:
•Triglycerides – main lipid component,
nonpolar/insoluble in water

Chylomicron (lipoprotein)
Chylomicron remnant
Exogenous Pathway
Apolipoprotein
Non-polar amino acids
Polar amino acids
Lipid Absorption: Triglycerides
Diglyceride
Monoglyceride
Lipid Absorption: Cholesterol
NPC1-L1 Receptor
Cholesteryl EsterCholesteryl
EsteraseCholesterol and fatty acid
Lipid Absorption: Phospholipids
Very Low Density Lipoprotein (VLDL)
VLDLIDLLDL
Endogenous Pathway
• Phospholipids – micellear structure
• Cholesterol – makes sure the lipoprotein is rigid enough
• CE - hydrophobic
• Apolipoprotein – stabilizes the structure
Hydrophobic – core substances
• A lipoprotein that is in triglycerides, can reflect light
and has the least density (lightest).
• Triglyceride, with absorbed cholesterol, phospholipid
and cholesteryl ester (Components) are assembled in the
form of chylomicron and must be in complex with
apolipoprotein.
• They are then released in the basal part of intestinal
cells towards the lamina propria, entering the lymphatic
capillaries (permeable).
Smaller version of chylomicrons. These are metabolized
in the liver, which is why it is expected for the plasma to
be clear-looking after eating.
• Absorption and digestion of dietary lipids.
• Lipoprotein lipase hydrolyzes triglycerides on the
chylomicrons generating fatty acids and glycerol.
• Newly synthesized chylomicrons in the
intestinelymphatic ductseventually enter the
circulation in the thoracic duct, draining in the
subclavian vein.
• In the tissues, chylomicrons bind to heparin sulphate
and other proteoglycans present in the capillaries of
different tissues.
• Binding to proteoglycan promotes interaction with
lipoprotein lipase.
• Chylomicron remnants are rapidly taken by the
hepatocytes (liver cells) and are broken down by
lysosomes into free cholesterol, fatty acids and amino
acids.
• Found on the surface of the lipoprotein
• Help maintain the integrity of the lipoprotein
• Amphipathic helix – protein substances that fold once in
contact with a polar/non-polar interface.
• Hydrophobic
• May interact with water
Are broken down because they are large through
pancreatic lipase.
If one fatty acid is removed, triglyceride will be…
If two fatty acids are removed.
• Absorbed by the action of the bile.
• Absorption is via the NPC1-L1 receptor
Blocked by people with hypercholesterolemia to manage
cholesterol/blood levels.
Absorbed through passive diffusion
• Acted upon by the phospholipase enzyme (removing one
fatty acid) releasing fatty acid and lysophospholipids.
• Enzyme breakdown: Pancreatic Lipase
• Transports hepatic-derived lipids
• Synthesized by the liver in times of fasting/starvation
• Transfers triglycerides from the liver to the peripheral
tissues
• Contains large amounts of TAG but not as much as
chylomicrons. Good source of energy.
• Plasma appears turbid (if the patient is undergoing
fasting)
• High intake is harmful! May cause plaque formation in
the walls of your arteries.
• Excess dietary intake of carbohydrates, saturated fatty
acids and trans fatty acids
• LDL (bad cholesterol) has high cholesterol content and
provides testes and others hormones.
• VLDL – once secreted in the blood, undergo a lipolytic
process similar to that of chylomicrons.
• VLDL loses core lipids in the action of lipoprotein lipase
and becomes VLDL remnants.
Elastic Cartilage

Low Density Lipoprotein (LDL)
High Density Lipoprotein
Discoidal HDL
Spherical HDL
HDLLCATHDL
Reverse Cholesterol Transport Pathway
Tangier Disease
Apolipoproteins
1. Apolipoprotein A1
2. Apolipoprotein B100
3. Apolipoprotein B48
4. Apolipoprotein C-III
5. Apolipoprotein E
• ½ of VLDL remnants gain cholesterol and eventually
become the IDL and LDL.
• ½ are taken up by the liver and are metabolized.
• Bad cholesterol, converted to steroid hormones.
• Once bound to receptors, the LDL are
endocytosedtransported to the lysosomes for
degradation/digestion.
• TAG component is acted upon by acid lipase to produce
glycerol and fatty acids (sources of energy)
• Smallest but most dense, highest protein content
• Transports cholesterol from the cells to the liver for
elimination or formation of bile acids.
• Secreted by the liver and small intestine
• Good cholesterol
• Has Apo-A1 (activator of lecithin cholesterol
acyltransferase)
• Newly synthesized HDL. Composed of Apo-A1
• Purpose: pick up small amounts of TAG and cholesterol
from the tissues to be transported to the liver.
Mature form, transports cholesteryl ester to the liver.
• Excess cholesterol from non-hepatic tissues is
transferred to the liver for metabolism and excretion into
the bile.
• Lipid-poor discoid HDL particles, produced in the liver
or the intestine, initiate the efflux of cholesterol and
phospholipids from cell membranes via interaction with
the adenosine triphosphate binding cassette transporter
A1 (ABCA1).
• Subsequent action of lecithin-cholesterol acyl
transferase (LCAT) esterifies cholesterol in preβ-HDL
particles and converts them to mature α-HDL particles.
• Mature HDL can deliver cholesterol to the liver either
directly via:
• (1) the scavenger receptor type B1 (SR-B1)
• (2) indirectly by exchange of cholesteryl esters to apoB-
containing particles for triglycerides (TG).
• Cholesteryl esters can be exchanged for triglycerides in
apoB-rich particles (LDL and VLDL) by cholesteryl ester
transfer protein (CETP).
• The uptake of apoB-rich particles via hepatic LDL
receptors enables the delivery of cholesterol to the liver
(approximately 50% of RCT).
• Reduced levels of HDL in the blood.
• Mutations to chromosome 9q31 lead to a defective
ABCA1 transporter. These mutations prevent the
ABCA1 protein from effectively transporting cholesterol
and phospholipids out of cells for pickup by ApoA1 in the
bloodstream. Causes an early onset of acute myocardial
infarction.
Bind lipids to form lipoproteins
• Produced by the liver and intestine
• Activator of LCAT enzyme
• Major protein component of HDL particles in plasma
• Chylomicrons secreted from the intestinal enterocyte
also contain apo A1, but it is quickly transferred to HDL
in the bloodstream.
• Used by the LDL to bind to the LDL receptors on the
cell membrane of human cells.
• Synthesized in the liver along with the synthesis of
VLDL
• Important in the assembly of VLDL and cellular uptake
of LDL
• Present in VLDL, IDL and LDL
• ApoB48 is identical to the amino-terminal 48% of
ApoB100
• involved in the synthesis, assembly and secretion of
chylomicrons
• Activator of lipoprotein lipase
• Present in chylomicrons, VLDL, IDL and LDL
• Facilitates the binding of lipoprotein remnants to the
 liver for elimination or metabolism.
• Present in chylomicrons and VLDL.

Adult Reference Range for Lipids

Analyte Reference Range
Total Cholesterol 140-200mg/dL (3.6-5.2 mmol/L)
HDL-C 40-75mg/dL (1.0-2.0 mmol/L)
LDL-C 50-130mg/dL (1.3-3.4 mmol/L)
Triglycerides 60-150mg/dL (0.7-1.7 mmol/L)

Blood levels of cholesterol increases with age. Women

have higher HDL and lower cholesterol than men due
to estrogen.
Puberty in men causes the lowering of HDL.
National Cholesterol Education Program
(NCEP)
Positive Risk Factors:
• Age > 45 years for men, > 55 years for females or
premature menopause.
• Family history of premature CHD
• Current cigarette smoking
Coronary Heart Disease Risk Factors by the NCEP
• Hypertension (BP>140/90 or taking anyihypertensive
drugs
• HDL-C concentration <40mg/dL (<1.0mmol/L)
• Diabetes mellitus = CHD risk equivalent
• Metabolic Syndrome (multiple metabolic risk factors)
Negative Risk Factors:
• HDL-C concentration > 60mg/dL (> 1.6mmol/L); its
presence removes one risk factor from the total count.
• Elevation of plasma cholesterol, trigylcerides or both
• Low HDL cholesterol level that contributes to the
development of antherosclerosis and other related
diseases.
Dyslipidemia • Can be caused by genetic abnormalities or
environmental factor or lifestyle imbalances. Others
occur secondary to other underlying disorders
• Arteries grow thick and stiff; restricting blood flow
to organs and tissues in the body.
• One of the causes of death and disability.
• Mortality rate has decreased through time due to
advancements in diagnosis and treatment and
awareness.
• Deposistion of cholesteryl esters in the arterial walls
that result to the formation of fatty streaks. (thin
streak of fats within macrophages within the
Arteriosclerosis subendothelial spaces).
• Injury signals from the growing fatty streaks or
plaque trigger the expression of adhesion proteins
which allow the migration of more macrophages,
platelets and lymphocytes
• Chronic inflammation results from repeated cycles of
injury
• Narrowing of the blood vessel causes the blood to
circulate in a nonlaminar manner under great
 pressure and this aggravates the plaque formation
• Some can burst and cause thrombosis
• Final event = occlusion of blood flow
Peripheral Vascular Disease If the plaque develops in the arteries of the arms or
legs.
Coronary Artery Disease Acute myocardial infarction
Cerebrovascular Disease Stroke