Lipids – Part 2

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 _________

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

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 – • Made in liver • Carries • HDL – • 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 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) • (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. 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-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 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. 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.

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 :

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