1. Lipids – Part 2
McCafferty

2. LIPID DIGESTION & ABSORPTION
Absorbable forms:

3. Remember “hydrolysis?”

4. Mouth
Mechanical: chewing, mixed w/saliva for lubrication
Chemical:

5. Stomach
Mechanical: peristalsis/churning ____________
Chemical:

6. 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 _________
one end “attracts and holds fat” while the other end is “attracted to and held by water.”

8. Once fat is emulsified into the liquid, enzymes can work:
Pancreas releases: pancreatic lipase
TG _________________________________
(DRAW BELOW:)

9. Lipid Absorption Small lipid fragments:
Glycerol and Short Chain FAs (SCFAs)
Absorbed directly into the bloodstream
Portal vein to liver
If absorbed into the blood, they’d separate from the watery fluids and disrupt blood flow.

12. Lipid Absorption Big lipid fragments
Monoglycerides and LCFAs need help!
If absorbed into the blood:
They need to be emulsified.

15. 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

16. Lymph vessel   
The tissues can extract what they need from the CMs.
CM remnants  

17. Lipoproteins -- Overview
Lipids bound to protein
Spherical structure –
“Shuttle”

19. 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

20. LDL – HDL – Made in liver Carries Made in liver & intestine
Associated w/ risk for CVD

23. 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

24. LDL cholesterol increases with
LDL to HDL ratio
Men:
Women:
LDL cholesterol increases with
HDL cholesterol increases with

25. STORAGE & USE OF FAT Overview: TG is main form of stored E in the body
Adipose –
When body needs fuel

27. Storing Fat TG in blood (in CMs and VLDL) INSULIN present
(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

28. Storing Fat
In adipose, TG  fat droplets

30. Storing Fat In adipose, TG  Adipose cells stretch to hold   fat
Once filled to max capacity, cells begin to multiply

31. 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

32. What kind of fat gets used for energy? What is triglyceride made of?
USING FAT TO MAKE ATP
What kind of fat gets used for energy?
What is triglyceride made of?

33. ______________
C-C C-C C-C
C-C-C
_____________
_____________
C-C
Krebs
ATP
ETS

34. 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

35. Therefore,

36. So what’s the point?
If we are out of glycogen and need to make glucose for those glucose-dependent tissues, we aren’t going to be able to use fatty acids to do it.

37. 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.

38. Cardiovascular Disease

39. 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

40. Stroke –blood flow to a part of the brain is cut off
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.

41. Atherosclerosis
Slow, progressive disease which begins in childhood and takes decades to advance.
Coronary arteries are most often affected.
(Most people have well-developed plaques by age 30)

42. “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

43. Thrombosis:
Embolism:

44. Angina:
pain, pressure, and tightness in chest, back, neck, and arms
caused by
Hypertension

45. The FOUR major risk factors: Smoking
 HDL,  BP, increases platelet stickiness (clots)
Hypertension
 cardiac work,  arterial damage
Risk :
want to expend at least 1000 kcals/week (45 min aerobics 4x/week or 10 miles of jogging)

46. 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.

48. 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

49. Homocysteine Strong + correlation w/premature disease
with inadequate B vitamins
(folate, B6 and B12 – fruits and veggies, lean meats)
Also:

50. 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
The Effects of Exercise (review recommendation) greatest benefit from aerobic activity – lowers LDL and raises HDL, strengthens heart and blood vessels, makes a leaner body, lowers blood pressure, improves peripheral circulation. Strength training also lowers LDLs and may decrease blood pressure. Some believe that physical activity should be the primary focus of CVD prevention.
LPL is more active, so more TG can be removed from the blood and used by the muscle for fuel

51. Dietary Prevention of Heart Disease
Fat
Saturated fat
Mono vs. Poly
Trans FAs
Sodium
Dietary Guidelines (review)
CHO > 55% of kcal, emphasis on cCHO (more fiber)
Sodium
Fat:
Reduce saturated fat intake, but not necessarily total fat
New research: Diet that provides up to 45% kcals from fat, as long as additional fat is monounsat’d, may lower LDL and not affect HDL
Pay attention to trans fatty acids – hydrogenated oils, mostly processed foods. Raise LDL and lower HDL, but to a lesser extent than SFAs
Alcohol intake: Moderate consumption increases HDL and prevents blood clot formation. However, 3+ drinks per day increases blood pressure and is associated w/increased mortality.
study on U.S. physicians showed lowest mortality w/2-6 drinks per week, and highest w/2 or more drinks per day.
levels for women are lower: lowest risk = 1-3 drinks per week.
Other protective dietary components:
Antioxidants (esp. Vitamin E)
Dietary Fiber (hi fiber diet is also high in folate and phytochemicals)

52. Alcohol
Antioxidants and Phytochemicals
Fiber
Fish
Soy