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final Flashcards

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1
Q

describe fatty acids

A

metabolic fuel; building blocks for membrane lipids
carboxylic acid with 4-22 carbon hydrocarbon chain
saturated or unsaturated (mono/poly)

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2
Q

describe FA IUPAC nomenclature

A

numbering of carbons starts from the carboxyl group
alpha carbon is second, omega is last on the chain regardless of length (eg ‘omega 3’ means first double bond is at 3rd carbon from methyl end)
IUPAC name comes from number of carbons (eg 16 C, hexadecane) and then replace ‘e’ with ‘oic’ (hexadecanoic acid aka palmitic acid)

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3
Q

how is triacylglycerol (TAG) synthesized

A

3 steps
1) convery G3P (glycerol 3-phosphate) to PA (phosphatidic acid) by adding 2 acyl chains to the two OH groups
2) hydrolysis of PA to get 1,2-diacylglycerol
3) convert DAG to TAG with DAG acyltransferase

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4
Q

what is SCD and what does it do

A

stearoyl-CoA desaturase
adds double bond to saturated FA (saturated fatty acyl-CoA –> monounsaturated fatty acyl-CoA)
uses NADPH

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5
Q

describe the stages of FA synthesis

A

1) transfer acetyl-CoA from mitochondria to cytoplasm
2) activation of acetyl-CoA to malonyl-CoA
3) FA synthesis, add 2 C at a time, 4 step elongation

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6
Q

where do you get acetyl CoA for FA synthesis

A

formed in mitochondria from bridge reaction and catabolism of AAs
not significant amount from FA degradation b/c synthesis and degradation are reciprocally regulated

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7
Q

describe the first step of FA synthesis

A

transport acetyl CoA to cytoplasm (made in mitochondria, whose membrane is impermeable to acetyl CoA)
convert to citrate with citrate synthase, transport, then use ATP citrate lyase to turn it back into acetyl CoA
uses 1 ATP and 1 NADPH

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8
Q

describe the formation of malonyl CoA for FA synthesis

A

activation of acetyl CoA via acetyl-CoA carboxylase
committed step in FA synthesis
2 step process
1) carboxybiotin intermediate formed
2) activated CO2 transferred to acetyl CoA to make malonyl CoA

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9
Q

describe acetyl CoA carboxylase

A

involved in activation of acetyl CoA to malonyl CoA, the committed step in FA synthesis
3 functional regions
biotin carboxylase: activates CO2 by attaching it to biotin
transcarboxylase: transfer CO2 to acetyl CoA, making malonyl CoA
biotin carrier protein; long flexible biotin arm rotates, carrying biotin carboxylase active site to transcarboxylase active site

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10
Q

describe the last of the three steps of FA synthesis

A

repeating 4 reactions via fatty acid synthase
condensation, reduction, dehydration, reduction again
each cycle has the acyl chain extended by 2 carbons
at 16 C (palmitate), it leaves the cycle

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11
Q

describe condensation in FA synthesis

A

catalyzed by beta-ketoacyl-ACP synthase
activated acetyl and malonyl groups joined to form acetoacetyl ACP, CO2 released

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12
Q

in FA synthesis, malonyl CoA is used to make acetoacetate. CO2 (one carbon) is lost in this process. Why then is a CO2 added to acetyl CoA to make malonyl CoA beforehand (activation)?

A

activated malonyl groups as opposed to acetyl groups makes the condensation reaction thermodynamically viable

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13
Q

describe the second stage in the fatty acid synthase pathway

A

reduction
acetoacetyl-ACP is reduced at C3 carbonyl to make D-3-hydroxybutyryl-ACP
uses (oxidizes) NADPH
done by KR (beta-ketoacyl-ACP reductase)

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14
Q

describe the third step in the fatty acid synthase pathway

A

dehydration
OH in D-3-hydroxybutyryl-ACP released as water; trans double bond formed, get crotonyl-ACP
done by beta-hydroxyacyl-ACP dehydratase

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15
Q

describe the final step of fatty acid synthase pathway

A

second reduction
trans bonds of crotonyl-ACP reduced (saturate) to form butyryl-ACP
catalyzed by enoyl-ACP reductase

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16
Q

what is the source of NADPH for FA synthesis

A

a) malate conversion to pyruvate by malic enzyme uses NADP+, making NADPH
b) pentose phosphate pathway makes 2 NADPH

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17
Q

describe FA elongation

A

palmitate is precursor for long chain FAs; have enzymes to catalyze this
same mechanism as synthesis (malonyl CoA adds 2C units via 4 reactions)

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18
Q

describe how unsaturated fatty acids are made

A

desaturases introduce double bonds into saturated chains
eg SCD turns stearoyl CoA to oleate (C18:1) and palmitoyl-CoA to palmitoleate (C16:1); both substrates to make DAG, TGs, cholesterol esters, phospholipids
mammals can’t make double bonds past C9
PUFAS in mammals derived from palmitoleate, oleate, dietary linoleate and linolenate

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19
Q

what are the steps of FA processing

A

mobilization (TAGs degraded to FAs and glycerol for transport to tissues)
activation (FAs activated and transported to mitochondria for degradation)
beta oxidation (FAs broken into acetyl CoA 2 C at a time and processed in TCA cycle

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20
Q

describe FA mobilization

A

overall process: lipase breaks TAG to FAs and glycerol

takes place on surface of lipid droplet in adipocyte
glucagon and epinephrine trigger lipolysis; trigger adenylate cyclase to make cAMP
PKA activated through cAMP; phosphorylates perilipin
this restructures fat droplet so TAG is more accessible, and releases ATGL cofactor to initiate mobilization

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21
Q

describe FA activation

Study These Flashcards
A

takes place in mitochondria, need membrane transporters to get in
2 steps via acyl CoA synthetase
1) FA reacts with ATP to make acyl adenylate, which enters mitochondria
2) sulfhydryl group of CoA attacks acyl adenylate to form acyl CoA and AMP

activated FAs can cross outer mitochondrial membrane through porin channels (voltage dependent)
to cross inner membrane they must link with carnitine to make acyl carnitine, then shuttled by translocase

22
Q

what do carnitine acyltransferase 1 and 2 do

Study These Flashcards
A

used to get activated FAs into mitochondria for oxidation
1 on outer mitochondrial membrane, 2 on matrix side
1 attaches acyl CoA to carnitine to make acyl carnitine so translocase can get it in matrix
2 uses CoA to reform the acyl CoA, carnitine shuttled back by translocase

23
Q

describe FA oxidation

Study These Flashcards
A

oxidize FAs to acetyl CoA, releasing high energy electrons to power oxidative phosphorylation
makes FADH2, NADH, acetyl CoA
4 stages
1) oxidation (acyl CoA to enoyl CoA by acyl CoA dehydrogenase)
2) hydration (hydrate double bond b/w C2 and 3 by enoyl CoA hydratase)
3) 2nd oxidation (convert hydroxyl group at C3 to keto group by L-3-hydroxyacyl CoA dehydrogenase)
4) cleavage (thiolysis of 3-kryoacyl CoA by thiol group of 2nd molecule of CoA by beta-ketothiolase)

24
Q

why is FA oxidation called beta oxidation

Study These Flashcards
A

2nd oxidation (step 3) takes place at the beta carbon (C3)

25
describe the energy production from FA oxidation
each cycle makes FADH2, NADH, and acetyl CoA palmitate needs 7 reaction cycles; in the 7th, c4-ketoacetyl CoA cleaved to 2 acetyl CoA, so you get 8 acetyl CoA, 7 FADH2, 7 NADH; all enter respiratory chain 8 acetyl CoA gets 80 ATP 7 FADH2 gets 10.5 ATP 7 NADH gets 17.5 ATP subtract 2 ATP for activation; net 106 ATP
26
how are ketone bodies used as fuel
metabolized to generate NADH and acetyl CoA acetoacertate is regulatory; high levels causes decrease of lipolysis rate don't generate as much ATO as FAs
27
describe the metabolic functions behind the ketogenic diet
decrease carbs, increase fat lack carbs needed to make acetyl CoA; body goes into starvation state, using ketone bodies for fuel (ketosis)
28
what is ketoacidosis
buildup of acidic ketone bodies; happens when body breaks down fat too fast; common in type 1 diabetes, potentially life threatening
29
when is a ketogenic diet useful
PDH deficiency; lactate acidosis; carb decrease from keto diet minimizes accumulation of lactate and increases source of acetyl CoA glucose transport deficiency; glucose can't go across blood brain barrier if deficient in the transporter, ketone bodies enter differently so keto diet helps normal function epilepsy; reduces seizures, not fully understood cancer: cancer cells upregulate glycolysis, so lack of carbs could starve them out diabetes: lack carbs, decrease need for insulin, reducing blood glucose, TAG levels, cholesterol levels, LDL levels risk: increased risk of kidney stones because of acidosis stopping calcium reabsorption in kidney
30
describe cholesterol de novo biosynthesis
3 stages in cytosol, start with acetyl CoA 1) synthesize isopentenyl pyrophosphate (includes rate limiting and committed step, HMG-CoA to mevalonate via HMG CoA reductase; after, multiple phosphorylation steps consuming 3 ATP to get a 5 carbon isoprene) 2) condensation of 6 isopentenyl pyrophosphate molecules to make squalene (overall reaction: C5 -> C10 -> C15 -> C30) 3) squalene cyclizes, converted to cholesterol
31
describe the role of cholesterol in SREBP signalling
high chol inhibits SCAP SREBP translocation, inhibiting expression of HMG CoA synthetase (involved in rate limiting and committed step of cholesterol synthesis; high cholesterol inhibits cholesterol synthesis)
32
what is the use of esterified cholesterol
free cholesterol is toxic; esterified for storage and transport
33
name 5 potential fates of cholesterol
sterol hormones vitamin D bile salts cell membranes lipoproteins
34
name some cholesterol derived sterol hormones
progesterone: prep uterus for implantation and pregnancy testosterone: male sex characteristics estradiol: female sex characteristics cortisol: a glucocorticoid, promote gluconeogenesis, glycogen synthesis, degradation of fats and protein aldosterone: mineralocorticoid, regulates sodium levels and blood pressure
35
what is feedforward stimulation
upstream metabolites activate downstream enzymes
36
what are the two types of allosteric regulation in metabolism
feedback inhibition (end product inhibits committed step) and feedforward stimulation
37
how is allosteric regulation of glycolysis done
via the energy state high energy inhibits glycolysis; pyruvate kinase step makes ATP, which inhibits PFK; also glucose 6 phosphate performs negative feedback on hexokinase low energy activates PFK; pyruvate kinase activated by fructose 1,6-bisphosphate via feedforward stimulation
38
does the presence of fructose-2,6-bisphosphate allosterically promote glycolysis or gluconeogenesis
promotes glycolysis; allosteric regulator of phosphofructokinase (PFK)
39
describe PFK2 regulation
covalently regulated; inhibited by phosphorylation protein kinase A phosphorylates and inhibits it, activating FBPase (glycolysis inactive) phosphoprotein phosphatase dephosphorylates it, activating it
40
describe pyruvate kinase regulation
covalent regulation inactivated by phosphorylation by PKA activated by dephosphorylation by phosphoprotein phosphatase
41
what does pyruvate kinase do
turns phosphoenolpyruvate and ADP to pyruvate and ATP
42
describe regulation of pyruvate dehydrogenase
covalent regulation; controls bridge reaction so controls TCA cycle activated when dephosphorylated by PDH phosphatase; happens when ADP and pyruvate inhibit PDH kinase inactive when phosphorylated by PDH kinase; happens in presence of NADH, acetyl-CoA, ATP
43
describe ChREBP
carbohydrate response element binding protein TF regulating glucose/lipid metabolism, activated by Xylulose-5-phosphate mediates expression of genes like pyruvate kinase, acetyl CoA carboxylase, FA synthase, etc
44
what is the cori cycle
separation of glycolysis into muscle and gluconeogenesis into liver, with blood in between; prevents futile cycling so metabolites are properly used glucose shuttled from liver to muscle, lactate shuttled from muscle to liver
45
describe GLUT1
glucose transporter in the blood, blood-brain barrier, and to a lesser extent the heart when deficient, brain no longer can use glycolysis as major energy source (glucose gets in through blood brain barrier) and relies on ketone bodies insulin-independent
46
describe GLUT2
glucose transporter in liver, pancreas, small intestine high Km, low affinity insulin-independent
47
describe GLUT3
glucose transporter in the brain, neurons, and sperm low Km, high affinity insulin independent
48
describe GLUT4
glucose transporter in skeletal muscle, adipose tissue, and heart insulin dependent
49
what is the metabolic consequence of insulin signalling being missing due to diabetes
causes an increase in cAMP; thus, cells constantly receive low glucose signal, inhibiting glycolysis and activating gluconeogenesis
50

BCEM 443 (2 decks)

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