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Biochemistry > Structure And Functions Of Fatty Acids And Triacylglycerols > Flashcards

Structure And Functions Of Fatty Acids And Triacylglycerols Flashcards

1
Q

Fatty acids

A

. Long chain (16-24c) carboxylic acids
. Saturated, monounsaturated, or polyunsaturated (omega-3/omega-6) w/ cis double bonds
. Essential fatty acids can’t be synthesized in humans

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2
Q

Triglycerides

A

3 fatty acids esterified to glycerol

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3
Q

Fatty acid functions

A

. Metabolic fuel that generate ATP during oxidation w/in mitochondria
. Metabolized to water soluble ketones in liver to be used as alternative fuel
. Involved in cell signaling process and components of structural lipids

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4
Q

Fatty acids biosynthesis locations

A

. Liver

. Lactating mammary glands

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5
Q

Rate limiting /regulated step in fatty acid biosynthesis

A

. Acetyl-CoA carboxylated to form Malonyl -CoA via acetyl-CoA carboxylase 1 (ACC1)
. ACC1 lipgenic enzyme in cytosol
. Biotin-dependent
. Requires ATP

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6
Q

Fatty acid synthase

A

. Multienzyme complex w/ 6 enzymatic domains
. Catalyzes stepwise formation of palmitic acid from malonyl-CoA
. Adds 2C units from malonyl CoA to form palmitic acid (16-C fully saturateD)
. 2 NADPH required
. Rxn: 8 acteyl-CoA (2C) + 7 ATP + 14NADPH -> palmitic acid [16:0]
. Needs

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7
Q

Other long-chain fatty acids formed from palmitic acid through ____

A

Elongation and desaturation rxns

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8
Q

Translocation of acetyl CoA from mitochondrial matrix. To cytosol

A

. Transported in form of citrate made by condensation of acetyl CoA and oxaloacetate by citrate synthase
. In cytosol, citrate is cleaved via ATP-citrate lyase to regenerate acetyl CoA

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9
Q

Allosteric activation/inhibition of ACC1

A

. Inter conversion of active polymeric form of ACC1 w/ inactive protomeric (subunit) form of enzyme
. Pos.: citrate (promotes polymerization of ACC1)
. Neg: long-chain fatty acids (promote depolymerization)

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10
Q

Reversible phosphorylation/dephosphorylation of ACC1

A

. Insulin stimulates phosphatase to dephosphorylate ACC1 to activate it

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11
Q

AMP-activated protein kinase (AMPK)

A

. Activated by AMP
. Promotes phosphorylation and inactivity of ACC1
. When ATP low, AMP high, ACC1 inhibited

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12
Q

Long-term regulation of ACC1

A

. Induction.inhibition of expression of ACC1 gene

. Regulated by dietary factors and hormones

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13
Q

Fatty acid elongation

A

Malonyl-CoA is 2C donor permitting elongation of pamitoyl-CoA by enzymes in smooth ER

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14
Q

Fatty acid desaturation

A

. Desaturase enzymes introduce cis-double bonds at carbons 4,5,6, and 9
. Most common desaturation btw C9-10 of palmitic acid and stearic (18:0) acid converting it to palmitoleic acid (16:1(9)) and oleic acid (18:1(9))
. need NADH and oxygen

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15
Q

T/F humans can’t introduce double bonds beyond C9 position

A

T

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16
Q

Essential fatty acids

A

. Linoleic acid (18:2(9, 12))
. Alpha-linolenic acid (18:3(9, 12, 15))
. Sometimes arachidonic acid (20:4(5,8,11,13)) but can technically be synthesized w/in body from linoleic acid

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17
Q

Desaturation and elongation of alpha-linolenicacid produces ____

A 
Eicosapentaenoic acid (20:5(5,8,11,14,17))
Docosahexaenoic acid (22:6(4,7,10,13,16,19))
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18
Q

Desaturation and elongation of linoleic acid forms ____

A

Omega-6 family of long-chain polyunsaturated acids

19
Q

Alpha-linolenic acid desaturation and elongation creates ___

A

Omega-3 family

20
Q

Substrates for pro- and anti-inflammatory eicosanoids

A

. Arachidonic acid (ARA)
. Eicosapentaenoic acid (EPA)
. These along w/ docosahexaenoic acid (DHA) accumulate in cell membranes in brain

21
Q

Storages of fatty acids as TAG

A

. Fatty acids in excess form triglycerides
. TAG packaged into VLDL particles and excreted into blood
. In muscle and adipose, lipoprotein lipase lipoprotein lipase hydrolyzes TAG present in circulating VLDL to release free fatty acids that are taken up into tissues and oxidized to form ATP or re-esterified to glycerol forming long-term energy reserve

22
Q

Limiting step of fatty acid oxidation and how is it regulated?

A

Carnitine shuttle by malonyl-CoA

23
Q

Lipases used in intracellular lipolysis

A

. Adipose triglyceride lipase (ATGL)
. Hormone-sensitive lipase (HSL)
. Monoglyceride lipase (MGL)

24
Q

How is low lipase activity in fed state achieved?

A

. ATGL not accos. W/ cofactors protein CGI-58 (complexed w/ perilipin A)
. HSL localized to cytosol

25
Q

What occurs when lipolysis is stimulated in fasted state w/ lipases

A

. Phosphorylation of perilipin A and HSL
. CGI-58 dissociates from perilipin and assoc. w/ ATGL to be fully active
. HSL activates and migrates to surface of lipid droplet where it assoc. w/ perilipin A

26
Q

In fasted state, fatty acids released from adipocytes bind to ___

A

Albumin and are transported in blood to tissues

27
Q

After transport into cells, how are fatty acids activated?

A

. Converted to fatty acyl-CoA by long-chain fatty acyl-CoA synthase that is assoc. w/ outer mitochondrial membrane
. Needs ATP to do this

28
Q

Carnitine shuttle

A

. Translocates fatty acids from cytosol to mitochondrial matrix
. Carnitine acyltransferse (CAT-1) on outer mitochondrial membrane transfers fatty acyl group from CoA to Carnitine
. Complex migrates through intermembrane space and inner mitochondrial membrane
. Carnitine acyltransferase II (CAT-II) releases fatty acid from carnitine and regenerates activated fatty acyl-CoA
. Rate limiting step of beta-oxidation

29
Q

T/F short and medium chain fatty acids (4-12C) enter mitochondria w/ carnitine shuttle

A

F, have independent mechanism

30
Q

Mitochondrial beta-oxidation

A

. Long-chain fatty acids oxidized through repeating series of 4 rxns of beta-oxidation
. Each cycle of beta-oxidation releases acteyl-CoA and generates FADH2 and NADH
Net: palmitoyl-CoA + 7FAD + 7H2O + 7NAD + 6CoA -> 8 acetyl-CoA + 7FADH2 + 7NADH + 7H (each cycle has 1 FADH2, NADH, and Acetyl CoA)

31
Q

MCAD deficiency

A

. Medium-chain acyl-CoA dehydrogenase (MCAD) is most common inborn error of fatty acid metabolism

32
Q

Ketone body location

A

. Fatty acids in liver cells converted to ketone bodies for metabolic fuel for non-hepatic tissues including brain

33
Q

How are fatty acids metabolized in muscle?

A

, metabolized to CO2 and H2O via beta-oxidation and TCA to generate ATP

34
Q

Ketogenesis in hepatocytes

A

. During extended fast
. Acetyl-CoA from fatty acid oxidation exceeds capacity of TCA to oxidize it to CO2 and H2O
. 3 Acetyl-CoA forms HMG CoA in mitochondria
. HMG-CoA forms acetoacetate
. Some Enters blood directly as fuel, most are reduced to beta-hydroxybutyrate (major ketone)
. Some acetoacetate spontaneously decarboxylates to acetone in blood which is excreted

35
Q

Ketolysis in peripheral tissues

A

. Beta-hydroxybutyrate and acetoacetate transported into mitochondrial matrix
. Converted back to acetyl CoA
. Catabolized by TCA cycle to generate ATP

36
Q

Enzyme that converts acetoacetate to acetoacetyl-CoA during ketolysis and where is is absent?

A

. SCOT enzyme
. Also called mitochondrial thiophorase
. NOT in liver so liver can’t use fatty acids as fuel

37
Q

Ketogenic amino acids

A

. Leucine and lysine

. Catabolism of carbon skeletons leads to ketone bodies

38
Q

If fatty acid has more than one double bond, they are spaced at ___ carbon intervals

A

3 carbon intervals

39
Q

Amount of contribution that biosynthesis of TAGs

A

Small because it is inefficient

40
Q

DHA and ARA have roles in ___

A

. Brain development
. Cortical visual acuity
. Cognition
. Infant development

41
Q

TAG formation

A

Glycerol phosphate + 3 acyl CoA + H2O -> TAG + 3 CoA + P

42
Q

ROle of ACC2 in regulation of fatty acid oxidation

A

. On outer mitochondrial membrane

. Makes malonyl CoA from acetyl CoA that inhibits CAT1 stopping fatty acid oxidation

43
Q

Net ATP from one palmitic acid

Biochemistry (64 decks)

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