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 s 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?
______________
_____________
_____________
Krebs
ETS
ATP

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-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 whats the point?



If we are out of glycogen and need to
make glucose for those glucose-
dependent tissues, we arent 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/HDLs
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

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