lipids – part 2 mccafferty. lipid digestion & absorption absorbable forms:
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Lipids – Part 2
McCafferty
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LIPID DIGESTION & ABSORPTION
Absorbable forms:
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Remember “hydrolysis?”
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MouthMechanical: chewing, mixed w/saliva for lubrication
Chemical:
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Stomach
Mechanical: peristalsis/churning
____________
Chemical:
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For digestion to continue, these fat droplets must be emulsifiedSmall IntestineFat droplets enter small intestinegallbladder contracts and releases __________
synthesized in the ______,
stored in the __________
made from _________
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Once fat is emulsified into the liquid, enzymes can work:
Pancreas releases: pancreatic lipase
TG _________________________________(DRAW BELOW:)
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Lipid AbsorptionSmall lipid fragments:
Glycerol and Short Chain FAs (SCFAs)Absorbed directly into the bloodstream Portal vein to liver
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Lipid AbsorptionBig lipid fragments
Monoglycerides and LCFAs need help! If absorbed into the blood:
They need to be emulsified.
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Big lipid fragments, cont.
Enter intestinal cell, re-form TGTG is incorporated into Lipoprotein carriers: Chylomicrons (CM)
Lipoprotein = lipid associated w/proteins
“Shuttle”
Protein and phospholipid act as emulsifiers for the other lipids
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Lymph vessel
The tissues can extract what they need from the CMs.
CM remnants
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Lipoproteins -- OverviewLipids bound to protein
Spherical structure – “Shuttle”
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Classes of LipoproteinsWhat 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
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LDL – Made in liverCarries
HDL – Made in liver & intestine
Associated w/ risk for CVD
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Recommended LevelsTotal cholesterol
For 30 yrs For 30 yrs (for kids 170 mg/dl)
LDL cholesterol HDL cholesterol Triglycerides (TG) *note controversy surrounding these numbers
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LDL to HDL ratioMen: Women:
LDL cholesterol increases with
HDL cholesterol increases with
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STORAGE & USE OF FATOverview:
TG is main form of stored E in the bodyAdipose – When body needs fuel
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Storing Fat
TG in blood (in CMs and VLDL)(need to get TG into adipose & muscle cells)
INSULIN presentActivates enzyme on blood vessel wall:LPL Lipoprotein LipaseLPL binds w/CM or VLDL and extracts TGBreaks down TG glycerol & 3FAs enter cell
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Storing FatIn adipose, TG fat droplets
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Storing Fat
In adipose, TG
Adipose cells stretch to hold fat
Once filled to max capacity, cells begin to multiply
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Mobilizing Stored Fat
TG in adipose; want to release FAs for E
Activates enzyme inside adipose cellHSL Hormone-sensitive lipase HSL breaks down TG G & FAs
FAs blood Hydrophobic, so bound to protein carrier: albumin cells metabolized for E
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USING FAT TO MAKE ATP
•What kind of fat gets used for energy?•What is triglyceride made of?
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______________
_____________
_____________
Krebs
ETS
ATP
C-C-C
C-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C
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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
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Therefore,
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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.
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Summary of ATP Production From Fat
Fat is comprised mainly of TG moleculesGlycerol and 3 FAs
Glycerol (3C) enters energy metabolism at pyruvateFAs (broken down to 2C units) enter at acetyl CoAFat can provide a very small amount of glucose form the glycerolComplete oxidation of TG yields ATP, CO2, H2O and body heat.
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Cardiovascular Disease
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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
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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.
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Atherosclerosis
Slow, progressive disease which begins in childhood and takes decades to advance.
Coronary arteries are most often affected.
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“Response to Injury Theory”Fatty streaks form along arterial wallsProliferation of smooth muscle cells, WBCs and calcium plaques Plaques cause the arteries to lose
elasticity
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Thrombosis:
Embolism:
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Angina: pain, pressure, and tightness in chest,
back, neck, and arms caused by
Hypertension
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The FOUR major risk factors:1. Smoking
HDL, BP, increases platelet stickiness (clots)
2. Hypertension cardiac work, arterial damageRisk :
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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.
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Other risk factors include:Heredity – parent or sibling male under 55, woman under 65Gender – male
women post menopause without estrogen
Age Stress and personality type
Type “A” personality, stress, depression
Elevated triglyceridesInversely correlated w/HDL’s
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HomocysteineStrong + correlation w/premature diseasewith inadequate B vitamins
(folate, B6 and B12 – fruits and veggies, lean meats)
Also:
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ExerciseStrengthens heart muscleLower body fat (also affects diabetes)Better glucose control blood pressure stressExercisers are less likely to be smokersImproved lipid profile (LDL, HDL) blood clotting
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Dietary Prevention of Heart Disease
Fat
Saturated fat
Mono vs. Poly
Trans FAs
Sodium
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Alcohol
Antioxidants and Phytochemicals
Fiber
Fish
Soy