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60 Cards in this Set
- Front
- Back
Triacylglycerols
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Storagelipid (3 fatty acid)
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Glycerophospholipids (cell membrane)
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Diglyceride (2 faty acids) + PO4 + Alcohol
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Sphingolipids (Phospholipids)`
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Sphingosine + Glyceride (1 fatty acid) + Choline
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Sphingolipid --- Plasmalogen ---
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most stable (long chain of C) ---- ester ---- s/t esle
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Sphingolipids (Glycolipids)
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Sphingosine + Glyceride (1 fatty acid) + Mono OR oligosacharides
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Isoprene
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Vit DEAK - Co Q
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Cholesterols
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Vit D - steroid hormone - Bile salt
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S1: Biles salt turns fat into
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Emulsified fat ------ Bile (liver- gall bladder- intestine) --- detergent (micelles)
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Bile contains .............
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cholic acid, taurocholic acid, glycocholate and others
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S2: Digestion - Lipase Converts triacylglycerols
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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)
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S3 Absorption and Reassembly
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Via epi cells (intestine) -- Free Glycerol -- Free Fatty Acids --- 2-monoacyl glycerols ---- THEN synthesis MORE TAG’s and less DAG’s === passing to Chylomicron
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Steps 4&5 – transport to target tissue
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TAG+cholesterol+apo-lipo-protein ---> Chylonmicron (in blood stream)
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Formation of Chylomicrons
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TAG’s and cholesterol esters ---- DAG’s and cholesterol (around) ---- “apoliproteins” (imbedded)
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Chylomicron as carriers and hooked to ---
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Lipoprotein Lipase along the capillary close to muscle-adipose-mamary to deliver the content and leave for LIVER as Chylomicron REMNANTS (LDL-VLDL-HDL)
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HDL - LDL composition
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LDL: 38% of Cholesterol ester vs 15% (HDL) --> hardening
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Steps 6, 7, & 8 – uptake of fat by tissue
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apoC-II in blood activate lipoprotein lipase and release FA in Myocyte (oxidized as fuel) or Adipocyte (reesterified for storage)
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Mobilization of Fat
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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
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Glycerol Metabolism
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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)
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Transport of the Fatty Acid into the Mitochondria
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A 3-step process and the rate limiting step ---- Once inside the mitochondria it is committed to b-oxidation.
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Step 1. Acyl-CoA formation ....
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catalyzed by fatty acyl-CoA synthetase on the outer mitochondrial membrane.
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Steps 2 and 3 - Carnitine Assisted Transport into Mitochondria
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Malonyl-CoA inhibits carnitine acyltransferase I. --- High concentrations of glucose increase the production of malonyl-CoA.
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Step 1 of b-oxidation – Oxidation by FAD
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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.
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Step 2 is hydration of The trans doubleAC bond
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This reaction is similar to fumarase.
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Step 3 – Oxidation of Alcohol by NAD+
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This reaction is similar to malate dehydrogenase of the TCA cycle. Inhibited by NADH
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Step 4 – Cleavage by thiolase
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Inhibited by acetyl-CoA
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b-oxidation
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takes off 2 carbons at a time
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From a 16 carbon fatty acid, you will get
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7 FADH2's, 7NADH's, and 8 acetyl-CoA's that can be fed into the citric acid cycle.
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b-Oxidation of Unsaturated Fatty Acids.
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There is 5th enzyme in this pathway to deal with unsaturation in the wrong position. This enzyme moves the double bond.
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There is a 6th enzyme to break conjugation
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This is a reduction by NADPH rather than an oxidation.
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b-Oxidation of Odd Numbered Fatty Acids.
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3 more enzymes are needed to deal with odd numbered fatty acids. --- Oxidation continues until there are only 3 carbons left yielding propionyl-CoA.
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Carboxylation by propionyl-CoA carboxylase to form D-methylmalonyl-CoA.
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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
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Epimerization by methylmalonyl-CoA epimerase to form
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... L-methylmalonyl-CoA.
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Rearrangement by methylmalonyl-CoA mutase to form succinyl-CoA.
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Requires vitamin B12
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Peroxisomes (flavoprotein dehydrogenase.)
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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.
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Ketone Body Formation in the Liver
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Condensation of two acetyl groups. The first step of ketone body formation is essentially the reverse of b-oxidation.
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Ketone Body BY products
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This reaction (also used in cholesterol synthesis) creates a 6 carbon product.
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Ketoneodies formation (Aceto-acetate)
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This reaction creates the first of the ketone bodies, acetoacetate.
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This reaction is similar to malate dehydrogenase of the TCA cycle.
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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.
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Ketone Body use in extrahepatic tissue
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Same enzyme used in synthesis -- Same as the 4th enzyme in b-oxidation
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Omega oxidation in endoplasmic reticulum
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making SUccinate and Adipate Adipic acid
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Biotin is Vitamin
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B7
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B1 - B2 - B3 ----- B5 - B6 - B7 ---- B9 ----- B12
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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)
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Gal stone block gall bladder
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no bile acid to emulsify fat
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Gal stone block common ducts
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block both bile and pancreatic enzymes (amylase-protease-lipase) --> can't digest anything
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Psncreatitis
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can cause by gall stone - pancreatic enz are back up and digest the pancreas --> leak out amylase
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Elevated serum amylase
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can cause by pancreatitis --> leak out from pancreas
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high fat diet
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fat can't be digested move to colons --> bact thrive and have more by products
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Orlistat
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(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
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Olestra
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fake fat can't be digested -- but bact can digest and thrive in colon
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Cholesterol absorption inhibitor
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can't digest cholesterol -- bact thrive -- cellulose can help bind to cholesterol and excrete out of the body
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Vitamin absorption
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don't have fat can't digest lipophilic vitamin DEAK
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Steatorrhea
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is the presence of excess fat in feces (no bile acid - no lipase - high fat diet)
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Carnitine
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fat carrier need CRT1 to attach fat to pass thru membrane and CRT2 to remove carnitine for recycling back out
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CRT 1 2 defect
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high fat in blood and Steatorrhea
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Hyperlipoproteinemia
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apoC2 defect (no activation onchylomicron) or Lipoportein lipase defects (no target for recognition)
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A lot of Epinephrine receptor on adipocytes (less glucacon -- more Insuline for fat storage)
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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)
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Serum albulmin
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FA carrier -- 50% (large amt) of serum protein
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S1 Fatty acyl-coA synthetase add ......
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CoA to FA (kick out H) -- add wt Carnitine (CRT1) and pass mito membrane (CRT2 strip Carnitine our and add CoA to FA again
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Malonyl-CoA (high insulin - high glucose) inhibit ...
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Carnitine acyltransferase 1 ---> stop transfer fat into mito for breaking down
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Step (4) of betapoxiation
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in mito
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