Lipids – Part 2
McCafferty
LIPID DIGESTION &
ABSORPTION
Absorbable forms:
Remember “hydrolysis?”
Mouth
Mechanical: chewing, mixed w/saliva for
lubrication
Chemical:
Stomach
Mechanical: peristalsis/churning
____________
Chemical:
For digestion to continue, these fat droplets
must be emulsified
Small Intestine
Fat droplets enter small intestine
gallbladder contracts and releases __________
synthesized in the ______,
stored in the __________
made from _________
Once fat is emulsified into the liquid,
enzymes can work:
Pancreas releases: pancreatic lipase
TG _________________________________
(DRAW BELOW:)
Lipid Absorption
Small lipid fragments:
Glycerol and Short Chain FAs (SCFAs)
Absorbed directly into the bloodstream
Portal vein to liver
Lipid Absorption
Big lipid fragments
Monoglycerides and LCFAs need help!
If absorbed into the blood:
They need to be emulsified.
Big lipid fragments, cont.
Enter intestinal cell, re-form TG
TG is incorporated into Lipoprotein carriers:
Chylomicrons (CM)
Lipoprotein = lipid associated w/proteins
“Shuttle”
Protein and phospholipid act as emulsifiers
for the other lipids
Lymph vessel   
The tissues can extract what they need from
the CMs.
CM remnants  
Lipoproteins -- Overview
Lipids bound to protein
Spherical structure –
“Shuttle”
Classes of Lipoproteins
What is denser, lipid or protein?
CM chylomicron –
made in intestinal cells
Transports ________TG from ________ to tissues
eg. adipose and muscle
VLDL – very low density lipoprotein
made in liver
Carries TG to tissues
LDL –
Made in liver
Carries
HDL –
Made in liver & intestine
Associated w/ risk for CVD
Recommended Levels
Total cholesterol
For  30 yrs
For  30 yrs
(for kids
 170 mg/dl)
LDL cholesterol
HDL cholesterol
Triglycerides (TG)
*note controversy surrounding these numbers
LDL to HDL ratio
Men:
Women:
LDL cholesterol increases with
HDL cholesterol increases with
STORAGE & USE OF FAT
Overview:
TG is main form of stored E in the body
Adipose –
When body needs fuel
Storing Fat
TG in blood (in CMs and VLDL)
(need to get TG into adipose & muscle cells)
INSULIN present
Activates enzyme on blood vessel wall:
LPL Lipoprotein Lipase
LPL binds w/CM or VLDL and extracts TG
Breaks down TG  glycerol & 3FAs  enter cell
Storing Fat
In adipose, TG  fat droplets
Storing Fat
In adipose, TG 
Adipose cells stretch to hold   fat
Once filled to max capacity, cells begin
to multiply
Mobilizing Stored Fat
TG in adipose; want to release FAs for E
Activates enzyme inside adipose cell
HSL Hormone-sensitive lipase
HSL breaks down TG  G & FAs
FAs  blood
Hydrophobic, so bound to protein carrier: albumin
 cells  metabolized for E
USING FAT TO MAKE ATP
What kind of fat gets used for
energy?
What is triglyceride made of?
______________
_____________
C-C-C
_____________
C-C
Krebs
ATP
ETS
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
C-C
Glycerol is converted to pyruvate
can either  glucose or acetyl CoA
/Krebs/ATP
Fatty Acids (too large to enter Krebs cycle)
can ONLY enter energy metabolism at
Therefore,
So what’s the point?
If we are out of glycogen and need to
make glucose for those glucosedependent tissues, we aren’t going to
be able to use fatty acids to do it.
Summary of ATP Production
From Fat
Fat is comprised mainly of TG molecules
Glycerol and 3 FAs
Glycerol (3C) enters energy metabolism at pyruvate
FAs (broken down to 2C units) enter at acetyl CoA
Fat can provide a very small amount of glucose form
the glycerol
Complete oxidation of TG yields ATP, CO2, H2O and
body heat.
Cardiovascular Disease
Cardiovascular Disease
– general term for diseases of the heart and
blood vessels
Coronary Heart Disease (CHD) – AKA Coronary
Artery Disease– lack of blood flow to the network of
blood vessels surrounding (and serving) the heart.
major cause: atherosclerosis.
Atherosclerosis – thickening and hardening of the
walls of the blood vessels 2 deposits of fatty
material (plaque)
esp. coronary and carotid arteries and abdominal
aorta
 Heart Attack – Lack of blood flow to the
heart muscle resulting in tissue damage
and sometimes sudden death
Stroke –blood flow to a part of the brain
is cut off
“brain attack.”
Usually due to atherosclerosis in the
carotid arteries.
Atherosclerosis
Slow, progressive disease which begins in
childhood and takes decades to advance.
Coronary arteries are most often affected.
“Response to Injury Theory”
Fatty streaks form along arterial walls
Proliferation of smooth muscle cells, WBCs and
calcium  plaques
 Plaques cause the arteries to lose elasticity



 Thrombosis:

 Embolism:

 Angina:
 pain, pressure, and tightness in chest, back,
neck, and arms
 caused by
Hypertension
The FOUR major risk factors:
1. Smoking
 HDL,  BP, increases platelet stickiness (clots)
2. Hypertension
 cardiac work,  arterial damage
Risk :
3. Elevated blood cholesterol
major lipid in plaque
4. Lack of regular exercise
Sedentary people (60% of US) have
double the risk of developing CVD as
active people.
Other risk factors include:
Heredity – parent or sibling male under 55,
woman under 65
Gender – male
women post menopause without estrogen
Age
Stress and personality type
Type “A” personality, stress, depression
Elevated triglycerides
Inversely correlated w/HDL’s
Homocysteine
Strong + correlation w/premature disease
with inadequate B vitamins
(folate, B6 and B12 – fruits and veggies, lean
meats)
Also:
Exercise
Strengthens heart muscle
Lower body fat (also affects diabetes)
Better glucose control
 blood pressure
 stress
Exercisers are less likely to be smokers
Improved lipid profile (LDL, HDL)
 blood clotting
Dietary Prevention of Heart Disease
Fat
Saturated fat
Mono vs. Poly
Trans FAs
Sodium
Alcohol
Antioxidants and Phytochemicals
Fiber
Fish
Soy