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54 Cards in this Set
- Front
- Back
a fatty acid with a double bond is labeled...
a fatty acid with 2 double bonds is labeled... |
-enoic acid
-dienoic acid |
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an omega 3 fatty acid has a double bond where?
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3 from end (not carboxyl end)
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4 major roles of fatty acids
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1) fuel molecules (stored as triacylglycerols)
2) building blocks of phospholipids and glycolipids 3) anchors for membrane and associated proteins 4) hormones and second messengers |
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triacylglycerols
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"fat": uncharged esters of fatty acids with glycerol
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3 types of hormones and second messengers that use fatty acids
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steroid hormones, prostaglandins, diacylglycerols (intracellular second messengers)
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fatty acids are derived from 2 sources:
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dietary fat and triacylglyceride storage
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lipases
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-synthesized in pancreas
-degrade dietary fats in intestines to fatty acids and monoacylglycerol for absorption into intestine -lipids aren't water soluble though, so they must be made accessible to lipases by bile salts |
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bile salts
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-derived from cholesterol
-suspend lipids by packaging into micelles -amphipathic molecules so can emulsify lipids (no charge in fats, but there is in f.a.s) |
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chylomicrons
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lipoprotein transport particles--deliver triacylglycerides to membrane-associated lipases mostly in adipose and muscle tissue
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after lipases degrade lipids to fatty acids and monoacylglycerol...
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triacylglycerols are re-synthesized in intestinal mucosal cells and packaged into chylomicrons
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triacylglycerides (stored fats) are processed in 3 stages:
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1) mobilization from adipose storage (degraded to f.a.'s and glycerol, released and transported)
2) processing in target tissues and cells (activation of f.a.s and transport into mitochondria) 3) energy generation in mitochondria (degradation of f.a.s into acetyl CoA and production of FADH2 and NADH) |
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serum albumin
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carrier of fatty acids in blood
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triacylglycerol lipase
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-key hormonal regulatory point in degradation of lipolysis
-epinephrine and glucagon induce lipolysis (activate cAMP-->PKA-->triacylglycerol lipase) -removes 1 fatty acid at a time from triacylglycerol |
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fate of glycerol after lipolysis
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glycerol kinase and glycerol phosphate dehydrogenase convert it to DHAP and GAP--can enter gluconeogenesis or glycolysis
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fatty acid activation for degradation
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-activated by addition of CoA on outer mitochondrial membrane
-2 step conversion of fatty acid to acyl CoA uses acyl CoA synthetase and requires ATP |
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acyl CoA
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-activated fatty acid
-must be transported across inner mitochondrial membrane because fatty acid oxidation occurs in matrix of mitochondria -conjugated to carnitine for transport across membrane |
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carnitine
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-zwitterionic alcohol used to transport acyl CoA across inner mitochondrial membrane
-acyl CoA is conjugated to carnitine to make acyl carnitine by carnitine acyltransferase I, it passes through transclocase, and is converted back to acyl CoA by carnitine acyltransferase II (maintains high energy transfer potential of acyl CoA) |
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beta-oxidation pathway
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-takes place in mitochondrial matrix
-one round yields acetyl CoA, a fatty acyl CoA n-2, FADH2 and NADH (from which energy is derived) |
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4 steps in each round of beta-oxidation
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1) oxidation by acyl CoA dehydrogenase
2) hydration by enoyl CoA hydratase 3) oxidation by L-3-hydroxyacyl CoA dehydrogenase 4) thiolysis by beta-ketothiolase |
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oxidation of acyl CoA
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-forms trans dbl bond between C2 and C3
-first source of ATP (~1.5) -enzyme is acyl CoA dehydrogenase (several isoforms of this enzyme for different chain lengths) -FAD is enzyme bound electron acceptor (electrons in FADH2 are transferred to ubiquinone in 3 steps then to cytochrome reductase) |
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acyl CoA DH step of fatty acid degradation (what happens to electrons)
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1) electrons from FADH2 prosthetic group of reduced acyl CoA are trasferred to 2nd flavoprotein: electron-transferring flavoprotein
2) ETF donates electrons to ETF:ubiquinone reductase (iron-sulfur protein) 3) ubiquinone is reduced to ubiquinol--delivers high potential electrons to 2nd proton-pumping site of respiratory chain |
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step 2 of beta-oxidation
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-hydration of dbl bond between C2 and C3
-enzyme is enoyl CoA hydratase (one size fits all) -yields no energy |
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step 3 of beta-oxidation
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-second oxidation reaction--conversion of hydroxyl at C3 into a keto group
-enzyme: L-3-hydroxyacyl CoA dehydrogenase (one size fits all, stereospecific) -yields 2.5 ATP from reduction of NAD |
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step 4 of beta-oxidation
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-cleavage of 3-ketoacyl CoA by thiol group of coenzymeA
-enzyme: beta-ketothiolase -yields acyl CoA (-2 C atoms) and acetyl CoA (latter can go into TCA cycle to yield ~10ATP) |
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oxidation of plamitate yields
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about 106 ATP (goes through 7 rounds of beta-oxidation)
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peroxisome and fatty acids
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can oxidize fatty acids but by different process: first step uses flavoprotein oxidase instead of dehydrogenase and produces H202 instead of reducing ETF
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oxidation of unsaturate fatty acids
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requires 2 additional enzymes
-odd-numbered dbl bonds: isomerase can fix -even-numbered dbl bonds: reductase + isomerase |
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if you have an odd number of C atoms in a fatty acid...
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(rare)
-in final round propionyl CoA and acetyl CoA are produced (instead of 2 acetyl CoA) -propionyl CoA is converted to succinyl CoA so can enter TCA cycle -rearrangement requires vit. B12 |
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coenzyme B12 structure
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corrin ring with cobalt in middle--group coming off cobalt toward you is the active part--gives away what it is:
cyanocobalamin: CN methylcobalamin: CH3 coenzyme B12: looks like nucleic acid |
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methyl malonyl CoA mutase
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-last step in conversion of propionyl CoA to succinyl CoA--unique reaction involving free radical because of Co
-homolytic cleavage: electron stays with Co and one electron stay with the C atom to generate free radical |
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if fatty acid oxidation exceeds capacity of TCA cycle, acetyl CoA...
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is diverted to form ketone bodies in the liver
conditions leading to formation of ketone bodies: prolonged fasting, high fat/low carb, diabetes |
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3 major ketone bodies
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-acetoacetate--can be converted to acetone (no ketone group) or D-3-hydroxybutyrate (by oxidation of NADH)
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3 things about ketone bodies as energy
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-heart muscle and renal cortex prefer acetoacetate to glucose
-brain normally uses glucose but in starvation or diabetes may adapt to using ketone bodies -liver produces ketone bodies but can't use them (doesn't have CoA transferase) |
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how ketone bodies are transformed into energy
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acetoacetate <-CoA transferase-> acetoacetyl CoA <-thiolase-> 2 acetyl CoA
(CoA is transferred from succinyl CoA to acetoacetate) |
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differences between fatty acid synthesis and degradation
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-degradation takes place in mitochondria, synth takes place in cytoplasm
-intermediates in degradation are covalently attached to CoA, synth=acyl carrier protein -oxidants in degradation: NAD+, FAD, reductant in synth: NADPH -chain is degraded 2 Cs at a time, split off as 2-C acetyl CoA, chain grows by 2 C's at a time, donated by 3-C malonyl CoA |
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committed step in fatty acid synthesis is...
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formation of malonyl CoA (2C donor in subsequent synthesis) by acetyl CoA carboxylase
converts acetyl CoA to malonyl CoA |
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3 enzymes that use biotin
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pyruvate carboxylase, propionyl CoA carboxylase, acetyl CoA carboxylase
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regulation of acetyl CoA carboxylase
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-glucagon and epinephrine promote inactivation, insulin promotes activation (not clear how)
-AMP-activated protein kinase phosphorylates carboxylase (inactivates it) when [AMP] is high; protein phosphatase 2A dephosphorylates carboxylase (activates it) -citrate activates carboxylase by converting enzyme from inactive dimer to filamentous active form; Palmitoyl CoA (abundant when there is excess of f.a.s does opposite) |
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malonyl CoA inhibits
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carnitine acyltransferase I--prevents conjugation of acyl CoA to carnitine, so can't get into mitochondria to undergo beta-oxidation in times of plenty
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CoA and acyl carrier protein
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different carriers, same business end (phosphopantetheine group)
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steps of fatty acid synthesis
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1) acetyla CoA is converted to malonyl CoA (regulatory step)
2) acetyl CoA and malonyl CoA are converted to acetyl ACP and malonyl ACP 3) acetyl ACP (2C) and malonyl ACP (3C) are condensed to acetoacetyl ACP (4C) 4) reduction with NADPH 5) dehydration 6) reduction with NADPH to butyryl ACP |
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synthesis of even vs. odd numbered fatty acids
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even numbered are derived from acetyl CoA
odd-numbered start with propionyl CoA |
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fatty acid synthase
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7 catalytic activities on one polypeptide chain
-has 3 domains -fatty acid chain gets passed around until it reaches length of C16 |
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domain 1 of fatty acid synthase
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-contains acetyl transferase, malonyl transferase, condensing enzyme
-substrate entry and condensation |
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domain 2 of fatty acid synthase
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-contains ACP, beta-ketoacyl reductase, dehydratase, enoyl reductase
-responsible for reduction |
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domain 3 of fatty acid synthase
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-contains thioesterase
-release of C16-ACP |
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what carries the fatty acid chain from one catalytic site to next?
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phosphopantetheinyl group of ACP
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modification of fatty acids
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-takes place in ER
-elongation: resembles fatty acid synthesis but fatty acyl chain is attached to CoA not ACP -desaturation: introduction of double bonds |
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essential fatty acids
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linoleate and linolenate (mammals lack enzyme to introduce double bonds at carbon atoms beyond C-9 in fatty acid chain)
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transport of acetyl CoA across mitochondrial membrane
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-acetyl CoA is synthesized in mitochondria, but f.a. synthesis uses it in cytosol
-citrate carries acetyl groups across mito membrane -for each acetyl CoA transported, one NADPH is generated -carnitine can also transport acetyl CoA but only long chains |
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antibacterial agents and fatty acid synthesis
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triclosan, isoniazid inhibit enoyl ACP reductase (step from crotonyl ACP to butyryl ACP--last reduction step)
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arachidonate
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(20:4), derived from linoleate, precursor for several classes of signaling molecules
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eicosanoids
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important fatty acid derivatives with specialized functions; arachidonic acid is precursor
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NSAIDs
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inhibit prostaglandin synthesis by blocking cyclooxygenase activity of prostaglandin synthase
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