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Biochem > Exam 1 Lipid synthesis > Flashcards

Exam 1 Lipid synthesis Flashcards

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1
Q

fatty acid synthesis occurs in

A

cytosol

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2
Q

hormone that stimulates fatty acid synthesis

A

insulin

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3
Q

prostethic group of ACC

A

biotin

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4
Q

substrates that ACC needs to make malonyl coa

A

Acetyl coa , bicarbonate and ATP

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5
Q

what happens when you eat raw eggs*

A

white stuff has avidin which steals biotin, ACC wont work so it would affect conversion of Acetylcoa into malonyl coa

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6
Q

how is mitochondrial Coa available in cytosol

A

Acetyl coa cant cross membrane
Citrate synthase converts OAA and Acetyl coa— citrate
citrate has transporter that takes it from mitochondria to cytosol
cytrate lyase- – citrate=== OAA and Acetyl coa
malate dehydrogenase– oAA– malate
malic enzyme—- malate ==== pyruvate Co2 NADPH

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7
Q

what happens when citrate is in excess

A

Citrate is transported via carrier from matrix into citosol and it can be used as precursor for acetyl coa synthesis

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8
Q

Name the reductant that is required for the fatty acid synthesis.

A

NADPH

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9
Q

substrate and product for malic enzyme

A

malate=== pyruvate co2 and NADPH

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10
Q

ACP vitamin derivative

A

phosphopantetheine
■ derivative of vitamin pantothenate (Vit B5)
■ a prosthetic group that a​nchors t​he growing fatty acid chain during
fatty acid synthesis

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11
Q

during palmitic acid synthesis what is used 7 times

A

Malonyl Coa

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12
Q

Name the enzyme domain that releases palmitate from the fatty acid synthase complex.

A

thioesterase I

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13
Q

Name the enzyme that is expressed during lactation in mammary gland that is relevant
to fatty acid synthesis.

A

Thioesterase II

causes premature release of shorter chain fatty acids

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14
Q

Fatty acids released by thioesterase II

A

Capric acid​(C­10)
○ Lauric acid (C­12)
○ Myristic acid (C­14)

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15
Q

two essential fatty acids

A

linoleic, linolenic

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16
Q

All naturally occurring double bonds of fatty acids are of cis­configuration.

A

true?

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17
Q

linoleic acid is precursor for

A

arachidonic acid

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18
Q

storage form of fatty acid

A

tryglyceride

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19
Q

tryglycerides stored

A

adipose tissue

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20
Q

Name the precursors for the synthesis of triglyceride.

A

fatty acids
○ CoA (coenzyme A)
○ Glycerol 3­phosphate

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21
Q

tryglycerides- fatty acids sterified to

A

glycerol backbone

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22
Q

Fatty acid synthesis occurs in ?

A

cytosol

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23
Q

in beta oxidation fatty, activted fatty acids are esterified to

A

carnitine

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24
Q

fatty acid breakdown occurs in

A

mitochondria

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25
3 energy related compounds in produced in beta ox
NADH FADH2 Acetyl coa
26
22. Name an enzyme that is located in the mitochondrial matrix that cleaves fatty acyl- carnitine.
carnitine acyltransferase II
27
Name a methylated fatty acid that is derived from dairy products.
phytanic acid
28
enzyme that uses cobalamin as coenzyme
methyl malonyl Coa mutase-- odd chain fatty acid metabolism | methionine synthase-- aAA metabolism
29
Name a three carbon compound that is formed from the oxidation of odd chain fatty acid.
propionly COA
30
Name two enzymes that convert propionyl CoA into succinyl CoA.
Propionyl CoA carboxylase (​has biotin as a prosthetic group) ○ Methyl malonyl CoA mutase (​has cobalamin as a prosthetic group)
31
28. Name two carboxylases that require biotin as a coenzyme.
acetyl CoA carboxylase ​(pg. 50) | ○ propionyl CoA carboxylase (​pg. 60)
32
compound catabolized by alpha oxidation
phytanic acid
33
why is phytanic acid NOT a substrate for ACC?
because it is substituted at the BETA carbon-- so it cant undergo beta oxidation
34
allosteric activator of ACC
citrate
35
allosteric inhibitor of ACC
fatty acyl coa ( product)
36
Carnitine acyl­transferase is inhibited by
malonyl coa
37
hormone that triggers catabolism of fats
glucagon
38
T/ F Phosphorylation of acetyl CoA carboxylase by protein kinase A inactivates the enzyme.
True- insulin activates a phostphate that DEphosphorylates ACC into itss active form
39
defect in Refsum disease
defficiency in alpha hydroxylase enzyme- cant degrade phytanic acid -- accumulates in plasma and nerve
40
SIDS deffective enzyme
medium chain fatty | acyl CoA dehydrogenases.​(pg. 66)
41
Name the two conditions that would result in methylmalonic acidemia​.​(pg. 66)
methylmalonyl CoA mutase ​is missing ○ deficiency of vitamin B12 ​(deoxyadenosyl c​obalamin​) ​(or conversion of startVitamin B12 into a coenzyme form is missing)
42
what happens in methylmalonic acidemia
acidemia​​­ causes metabolic acidosis and mental retardation due to the impaired metabolism of odd chain fatty acids
43
define obesity
obesity ​­ ​BMI (body mass index) greater than 30 kg/m2
44
39. Name a natural & an artificial compound that inhibits fatty acid synthase.
natural inhibitor ­ cerulenin | ○ artificial inhibitor ­ C75 (analog of cerulenin)
45
Malonyl CoA inhibits the production of a neuropeptide hormone called ____
NPY
46
T/F neuropeptide y signals inhibition of feeding?
??? false
47
describe diabettic ketoacidosis
Occurs when blood concentrations of acetoacetic acid & beta­hydroxybutyric acid (ketone bodies) are high. ○ These compounds are strong acids, resulting in acidosis.
48
DKA conditions similar to what? | what is the ratio of glucagon insulin?
``` the conditions are very similar to ​starvation ​because ​glucagon/insulin ratio is high (i.e. high glucagon, or low insulin) ```
49
Two enzymes that convert alcohol into acetate
alcohol dehydrogenase | ○ aldehyde dehydrogenase
50
Reductant produced in oxidation of alcohol
NADH
51
compounds metabolised by omega oxidation pathway
C 6-10 capric acid (C10) ■ caprylic acid (C8) ■ caproic acid (C6)
52
how many ATP used in omega oxidation
-4
53
Explain why fat storage is energetically better compared to glycogen?
fatty acids hold more amount of energy per storage mass because it can be stored in anhydrous environment
54
Explain how ketone bodies can serve as an energy source in brain during starvation?
Ketone bodies are able to cross the blood­brain barrier (wikipedia) ○ This means that ketone bodies a​re a direct energy source​for the brain
55
Explain why carnitine palmitoyltransferase I deficiency​leads to hypoketosis?​
carnitine palmitoyltransferase I (CPT I) converts palmitoyl CoA to palmitoyl­carnitine so that it can be transported from the cytosol into the mitochondria for oxidation. ○ Deficiency ​in carnitine ​or carnitine acyltransferase​→ can’t metabolize long­chain fatty acids (palmitic acid) → muscle weakness and
56
ketone bodies
acetoacetate beta hydroxy butyric acid, acetone
57
hypoketosis due to
LOW levels of ketone bodies
58
ketoacidosis due to
High levels of keone bodies
59
53. Is the NADH/NAD+ ratio high or low in alcoholics? | what does it do
high | promotes fatty liver thru inhibition of gluconeogenesis and fatty acid oxudation
60
What are omega­3 and omega­6 fatty acids?
``` Counting from the end of the carbon chain, FA with a double bond after the 3rd and 6th carbons respectively ○ Omega 3 FA = Linolenic acid ○ Omega 6 FA ​= Linoleic acid ○ essential fatty acids ```
61
Describe the citrate lyase catalyzed reaction. (pg. 49)
CoA + citrate + ATP → oxaloacetate + acetyl CoA + ADP
62
Can carbon skeleton from C­17 fatty acid oxidation enter gluconeogenic pathway? If yes, explain how?
Yes, because oxidation of odd chain fatty acids produces 1 molecule of propionyl CoA which is converted to succinyl CoA, so this is an anapleurotic reaction because it generates a TCA cycle intermediate. Succinyl CoA then eventually gets converted to oxaloacetate, which is an intermediate in gluconeogenesis
63
Can carbon skeleton from C­16 fatty acid oxidation enter gluconeogenic pathway? If yes, explain how?
No, because oxidation of a C­16 fatty acid chain produces only acetyl CoA. Acetyl CoA is then released from TCA cycle as carbon dioxide, so this reaction is NOT anapleurotic because it does not replenish TCA cycle intermediates. Thus, gluconeogenesis cannot occur because oxaloacetate is not made
64
Excretion of higher methylmalonic acid through urine is a sign of what vitamin deficiency?
Cobalamin
65
compound has sweet odor in type I
Ketone bodies
66
Explain the rationale behind the ketoacidosis in alcoholics.
Increased alcohol consumption will lead to conversion of ethanol to Acetyl CoA through a series of reactions (page 66). Increased amount of acetyl CoA will cause the liver to produce large amounts of ketone bodies which lowers blood pH and the result is ketoacidosis.
67
66. HIgh NADH/NAD+ in alcoholics results in the production of _____
3­hydroxybutyrate (Beta­hydroxybutyrate)
68
A person with a deficiency of vitamin B12 is recommended to avoid what type of food?
Alcohol
69
Biotin defficiency cant metabolize?
odd chain fatty acids

Biochem (10 decks)

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