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60 Cards in this Set

  • Front
  • Back
Triacylglycerols
Triacylglycerols
Storagelipid (3 fatty acid)
Glycerophospholipids (cell membrane)
Glycerophospholipids (cell membrane)
Diglyceride (2 faty acids) + PO4 + Alcohol
Sphingolipids (Phospholipids)`
Sphingolipids (Phospholipids)`
Sphingosine + Glyceride (1 fatty acid) + Choline
Sphingolipid --- Plasmalogen ---
most stable (long chain of C) ---- ester ---- s/t esle
Sphingolipids (Glycolipids)
Sphingolipids (Glycolipids)
Sphingosine + Glyceride (1 fatty acid) + Mono OR oligosacharides
Isoprene
Isoprene
Vit DEAK - Co Q
Cholesterols
Cholesterols
Vit D - steroid hormone - Bile salt
S1: Biles salt turns fat into
S1: Biles salt turns fat into
Emulsified fat ------ Bile (liver- gall bladder- intestine) --- detergent (micelles)
Bile contains .............
Bile contains .............
cholic acid, taurocholic acid, glycocholate and others
S2: Digestion - Lipase Converts triacylglycerols
S2: Digestion - Lipase Converts triacylglycerols
diacylglycerols, monoacylglycerols, free fatty acids and glycerol. ------ Majority are 2-monoacyl glycerols and free fatty acids. --------------- carboxylate - soap molecule (de-protonated by the high pH in intestine)
S3 Absorption and Reassembly
S3 Absorption and Reassembly
Via epi cells (intestine) -- Free Glycerol -- Free Fatty Acids --- 2-monoacyl glycerols ---- THEN synthesis MORE TAG’s and less DAG’s === passing to Chylomicron
Steps 4&5 – transport to target tissue
Steps 4&5 – transport to target tissue
TAG+cholesterol+apo-lipo-protein ---> Chylonmicron (in blood stream)
Formation of Chylomicrons
Formation of Chylomicrons
TAG’s and cholesterol esters ---- DAG’s and cholesterol (around) ---- “apoliproteins” (imbedded)
Chylomicron as carriers and hooked to ---
Chylomicron as carriers and hooked to ---
Lipoprotein Lipase along the capillary close to muscle-adipose-mamary to deliver the content and leave for LIVER as Chylomicron REMNANTS (LDL-VLDL-HDL)
HDL - LDL composition
HDL - LDL composition
LDL: 38% of Cholesterol ester vs 15% (HDL) --> hardening
Steps 6, 7, & 8 – uptake of fat by tissue
Steps 6, 7, & 8 – uptake of fat by tissue
apoC-II in blood activate lipoprotein lipase and release FA in Myocyte (oxidized as fuel) or Adipocyte (reesterified for storage)
Mobilization of Fat
Glucagon (low glucose) and Epinephrine (high stress) induce lipolysis. ----- activate Gs proteins (serpentine receptor) and increase (adenylate cyclase) ------ cAMP-dependent protein kinase phosphorylates hormone-sensitive triacylglycerol lipase. ----- Free fatty acids are released from the TAG's
Glycerol Metabolism
Glycerol Metabolism
5% ATP --- Glycerol kinase phosphorylate to (L-glycerol-3-phosphate) --- G-3-P-deH oxidate to diHacetone phosphate ---- triose phosphate isomerize to D-glyceraldehyde-3-phosphate (glycolysis pathway)
Transport of the Fatty Acid into the Mitochondria
Transport of the Fatty Acid into the Mitochondria
A 3-step process and the rate limiting step ---- Once inside the mitochondria it is committed to b-oxidation.
Step 1. Acyl-CoA formation ....
Step 1. Acyl-CoA formation ....
catalyzed by fatty acyl-CoA synthetase on the outer mitochondrial membrane.
Steps 2 and 3 - Carnitine Assisted Transport into Mitochondria
Steps 2 and 3 - Carnitine Assisted Transport into Mitochondria
Malonyl-CoA inhibits carnitine acyltransferase I. --- High concentrations of glucose increase the production of malonyl-CoA.
Step 1 of b-oxidation – Oxidation by FAD
Step 1 of b-oxidation – Oxidation by FAD
Removal of 2 hydrogens -- This enzyme is similar to succinate dehydrogenase and FAD is permanantely bound to the enzyme. -- The electrons from this reaction are fed directly to the electron-transferring flavoprotein (ETFP), a protein that the acyl-CoA dehydrogenase is bound to.
Step 2 is hydration of The trans doubleAC bond
Step 2 is hydration of The trans doubleAC bond
This reaction is similar to fumarase.
Step 3 –   Oxidation of Alcohol by NAD+
Step 3 – Oxidation of Alcohol by NAD+
This reaction is similar to malate dehydrogenase of the TCA cycle. Inhibited by NADH
Step 4 – Cleavage by  thiolase
Step 4 – Cleavage by thiolase
Inhibited by acetyl-CoA
b-oxidation
b-oxidation
takes off 2 carbons at a time
From a 16 carbon fatty acid, you will get
From a 16 carbon fatty acid, you will get
7 FADH2's, 7NADH's, and 8 acetyl-CoA's that can be fed into the citric acid cycle.
b-Oxidation of Unsaturated Fatty Acids.
b-Oxidation of Unsaturated Fatty Acids.
There is 5th enzyme in this pathway to deal with unsaturation in the wrong position. This enzyme moves the double bond.
There is a 6th enzyme to break conjugation
There is a 6th enzyme to break conjugation
This is a reduction by NADPH rather than an oxidation.
b-Oxidation of Odd Numbered Fatty Acids.
3 more enzymes are needed to deal with odd numbered fatty acids. --- Oxidation continues until there are only 3 carbons left yielding propionyl-CoA.
Carboxylation by propionyl-CoA carboxylase to form D-methylmalonyl-CoA.
Carboxylation by propionyl-CoA carboxylase to form D-methylmalonyl-CoA.
This is a biotin requiring reaction. --- bicarbonate and ATP are used in this reaction ---- ADP and Pi are produced in this reaction. ---- This reaction is similar to pyruvate carboxylase
Epimerization by methylmalonyl-CoA epimerase to form
Epimerization by methylmalonyl-CoA epimerase to form
... L-methylmalonyl-CoA.
Rearrangement by methylmalonyl-CoA mutase to form succinyl-CoA.
Rearrangement by methylmalonyl-CoA mutase to form succinyl-CoA.
Requires vitamin B12
Peroxisomes  (flavoprotein dehydrogenase.)
Peroxisomes (flavoprotein dehydrogenase.)
electrons are passed to molecular oxygen making peroxide -- Neutralization of the hydrogen peroxide is dependent on catalase. -- A high fat diet would result in an increased production of peroxizomal enzymes and consequently an increase in peroxide and potentially hydroxyl radicals.
Ketone Body Formation in the Liver
Ketone Body Formation in the Liver
Condensation of two acetyl groups.  The first step of ketone body formation is essentially the reverse of b-oxidation.
Ketone Body BY products
Ketone Body BY products
This reaction (also used in cholesterol synthesis) creates a 6 carbon product.
Ketoneodies formation (Aceto-acetate)
Ketoneodies formation (Aceto-acetate)
This reaction creates the first of the ketone bodies, acetoacetate.
This reaction is similar to malate dehydrogenase of the TCA cycle.
This reaction is similar to malate dehydrogenase of the TCA cycle.
The problem with ketone bodies is that they are very acidic causing acidosis (lowering of blood pH). The acetoacetate can both spontaneously and enzymatically decarboxylate to acetone which is toxic.
Ketone Body use in extrahepatic tissue
Ketone Body use in extrahepatic tissue
Same enzyme used in synthesis -- Same as the 4th enzyme in b-oxidation
Omega oxidation in endoplasmic reticulum
Omega oxidation in endoplasmic reticulum
making SUccinate and Adipate Adipic acid
Biotin is Vitamin
B7
B1 - B2 - B3 ----- B5 - B6 - B7 ---- B9 ----- B12
Vitamin B1 (thiamine) -- Vitamin B2 (riboflavin) --- Vitamin B3 (niacin or niacinamide) ---- Vitamin B5 (pantothenic acid) ----- Vitamin B6 (pyridoxine, pyridoxal, or pyridoxamine, or pyridoxine hydrochloride) --- Vitamin B7 (biotin) ---- Vitamin B9 (folic acid) ---- Vitamin B12 (various cobalamins; commonly cyanocobalamin in vitamin supplements)
Gal stone block gall bladder
no bile acid to emulsify fat
Gal stone block common ducts
block both bile and pancreatic enzymes (amylase-protease-lipase) --> can't digest anything
Psncreatitis
can cause by gall stone - pancreatic enz are back up and digest the pancreas --> leak out amylase
Elevated serum amylase
can cause by pancreatitis --> leak out from pancreas
high fat diet
fat can't be digested move to colons --> bact thrive and have more by products
Orlistat
(lipase inhibitor ) not prevent fat break out (digestion) --> less calories BUT shouldNOT eat lot of fat (undigested --> similar to high fat diet --> fed bact in colon) --> can't take vit (vit in fat) that's y
Olestra
fake fat can't be digested -- but bact can digest and thrive in colon
Cholesterol absorption inhibitor
can't digest cholesterol -- bact thrive -- cellulose can help bind to cholesterol and excrete out of the body
Vitamin absorption
don't have fat can't digest lipophilic vitamin DEAK
Steatorrhea
is the presence of excess fat in feces (no bile acid - no lipase - high fat diet)
Carnitine
fat carrier need CRT1 to attach fat to pass thru membrane and CRT2 to remove carnitine for recycling back out
CRT 1 2 defect
high fat in blood and Steatorrhea
Hyperlipoproteinemia
apoC2 defect (no activation onchylomicron) or Lipoportein lipase defects (no target for recognition)
A lot of Epinephrine receptor on adipocytes (less glucacon -- more Insuline for fat storage)
bind to hepserpetine receptor -- Gs dissociate -- AC ATP - cAMP - pKA -- P trygly lipase (to activate) break down tryglycerin in a very SLOW rate (low muscle prefer fat - has less glycogen -> bulky is skinny)
Serum albulmin
FA carrier -- 50% (large amt) of serum protein
S1 Fatty acyl-coA synthetase add ......
CoA to FA (kick out H) -- add wt Carnitine (CRT1) and pass mito membrane (CRT2 strip Carnitine our and add CoA to FA again
Malonyl-CoA (high insulin - high glucose) inhibit ...
Carnitine acyltransferase 1 ---> stop transfer fat into mito for breaking down
Step (4) of betapoxiation
in mito