Lipids Flashcards
What are lipids only soluble in?
Organic solevents
What are the essential FA? and what happens if they’re defficient?
A-linolenic acid (n3) - decrease in IQ and visual/retinal activity
linoleic acid (n6) - dermatitis, decrease in growth and reproductive maturity.
How do we make EFA?
We must desaturate and elongate to get FA from metabolites.
linoleic acid –> arachidonic acid –> pro inflammatory eicosanoid
a-linoleic –> eicosapentaenoic acid –> anti inflammatory eicosanoid
What does FA have?
hydrophobic tail and hydrophilic head group
FA naming: delta vs omega
Delta = numbering starts from carboxyl end. ie. 18:2delta^9,12
Omega = numbering starts from FA end. ie. 18:2n^6
What are TAGs?
main dietary and storage lipid
ester bonds
3FA + glyceride
What is a phospholipid?
more polar than TAG –> amphipathic
membranes
what is a sterol?
cholesterol ester
bile acid production
Lipid digestion: mouth
lingual lipase continously secreted (not rlly digested here)
lipid digestion: stomach
gastric lipase and lingual lipase = stable at low pH
lipid digestion: liver and gallbladder
make bile acids from cholesterol and storage of bile acids - emulsify lipids (released by hormones) because not soluble in water. This makes mixed micelles. the mixed micelles can access spaces between mv in the intestine by carrier mediated transporters.
lipid digestion: SI
pancreatic enzymes - pancreatic lipase, cholesterol esterase (breaks ester bond), and phospholipase (BBE)
Describe enterohepatic circulation
most bile is reabsorbed and only a little is lost in feces. soluble fiber reduces effeciency of enterhepatic circualtion which is good bcs we want more cholesterol to be lost to feces so your body can increase endrogenous production.
Describe lipid absorption.
mix micelles have to break down and then form back up to go to the lymphatic (lacteal) system.
Lipid transport: how are lipoproteins classified?
ratio to protein (density)
specific apolipoprotein content (Apo- receptor interations)
Lipid transport: chylomicron/CR
high lipid low protein
ApoB-48, ApoC, ApoE
Lipid transport: VLDL
high lipid low protein
ApoB-100, ApoC, ApoE
Lipid transport: LDL
bad cholesterol - relative to VLDL, protein to lipid ratio increases
ApoB-100, ApoC, ApoE
Lipid transport: HDL
good cholesterol - low lipid high protein
ApoA family
Describe chylomicrons.
They enter the lymphatic system before entering the blood. Dietary lipids are availble to adipose tissue and muscle before arriving at blood.
Chylomicrons: LPL
LPL (lipoprotein lipase) is located on the surface of the endothelial cells lining small blood vessels and capillaries. LPL is only expressed in muscle and adipose tissue and is activated by ApoC in chylomicrons and LPL hydrolyses the TAG in chylomicrons –> CR. This is insulin regulated.
LDL
Delivers cholesterol to for essentiality and to unwanted places.
VLDL is the main transporter of newly synthesized hepatic TAG. The ApoE and ApoB-100 receptors on LDL initiates the liver to take up LDL via receptor mediated endocytosis.
HDL
more cholesterol returning to liver through reverse cholesterol transport. But first LCAT (lectin-cholesterol) esterfies a FA to cholesterol to make a mature HDL. This can go right to liver via SR-B1 (scavenger receptor B1) which is an HDL receptor into the liver, or HDL–>VLDL + LDL by CETP (cholesterol ester transfer proteins) which transfers cholesterol ester from HDL to VLDL or LDL.
3 fates of cholesterol
- converted into bile acids to replenish
- eliminated as feces
- packaged into VLDL and send around body
What will happen to those with high blood cholesterol if you decrease dietary cholesterol?
Decrease LDL
Where do lipids fit into the previously discussed metabolic pathways: gluconeogensis
(inhibited by insulin) lipase hydrolyses ester linkages (lipolysis). In adipose tissue HSL (hormone sensitive lipase) cleaves a FA from glycerol backbone. This complete breakdown of 1TAG = 1 glycerol and 3 FA. The glycerol can go to glycolysis or gluconeogenesis and the FA can go to Boxid to generate E.
Beta oxidation.
each round of B-oxidation removes 2 carbons and produces 1 NADH and 1 FADH2. ie. 10 carbon FA goes through 4 rounds of b oxidation and produces = 4 nadh and 4 fadh2 = (4x3) + (4x2) =20ATP
Krebs cycle.
net energy produced = 3NADH + 1FADH + 1GTP = (3x3) + (1x2) + (1x1) = 12 ATP per 1 acetyl CoA
Combine B oxidation and krebs. How many ATP are produced by complete oxidation of a 10C FA.
(12 x 5) - from krebs cycle acetyl CoA (you get 5 acetyl CoA from a 10C FA
+
(20) - from 4 rounds of b oxidation that produces 4 nadh and 4 fadh2 each
= 80ATP
