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Biochemistry > Fatty Acid and TAG Catabolism > Flashcards

Fatty Acid and TAG Catabolism Flashcards

1
Q

what are the 2 lipases of F.A?

A

Hormone sensitive lipases and lipoprotein lipases

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2
Q

hormone sensitive lipases ?

A

release fatty acid from adipose for energy

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3
Q

lipoprotein lipases

A

release FA from lipoproteins for storage in adipose & usein other tissues

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4
Q

LPL diffuse into ?

A

inside adipose tissue cells..TAGs are resynthesized and stored for energy

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5
Q

HSL diffuse into ?

A

plasma and bind to abumin and are taken ti liver and degraded for energy

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6
Q

Activation of HSL

A 
Primary msg (Glucagon, epinephrine, ACTH) bind to membrance receptor
adenyl cyclase is activated 
cAMP increases 
Protein kinase activated 
Phosphorylates  "activates" HSL
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7
Q

what inhibits HSL ?

A

Insulin by dephosphorylation

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8
Q

activation of LPL

A

Apolipoprotein C2 is on surface of lipoprotein
LPL is on endothelial surface (in adipose, cardiac and skeletal m.)
when Lipoprotein gets close to surface Apo CII associates with LPL Causing it to become active

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9
Q

chylomicrons

A

Transport dietary lipid from intestine to adipose

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10
Q

Lipoproteins

A

Transport lipid between liver and other tissues.

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11
Q

albumin

A

transport Fatty Acids from adipose to liver

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12
Q

ketone bodies

A

Transported in solution in plasma. (i.e. from liver to skeletal + cardiac tissues)

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13
Q

VLDL

A

Primarily transports—–TAG from liver to adipose and other tissues (also taken up by liver)

~95% lipid….apo C-II, C-III, B-100, E

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14
Q

LDL and Composition

A

Primarily transports——- cholesterol to tissues (also taken up by liver)
~80% lipid….apo C-II, C-I, B-100, E

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15
Q

HDL and composition

A

Primarily transports——- cholesterol from tissues to liver

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16
Q

IDL and composition

A

Primarily transports——– cholesterol to tissues via conversion to LDL (also taken up by liver)

~80% lipid….apo C-II, C-III, B, E

17
Q

net energy yield from palmitate beta oxidation

A

7NADH –>10.5 ATP
7FADH2–>17.5 ATP
8 ACETYL CoA –>80 ATP
Subtotal 108 ATP

18
Q

CAT 1 are inhibited by

A

malonyl CoA which stops formation of acylcarnitine

19
Q

beta- hydroxy CoA DH inhibited by

A

NADH

20
Q

Thiolase inhibited by

A

acetyl coa

21
Q

lo energy charge creates ?

A

high isocitrate DH, low citrate … decrease fatty acid synthesis

22
Q

High energy creates

A

low isocitrate DH, high citrate …. increased FA Synthesis

23
Q

pathway by which cis containing double bonds enter b oxidation

A 
Enoyl CoA Hydratase
Beta-hydroxy FA CoA racemase
Propionyl CoA CO2lase
Methylmalonyl CoA racemase
Methylmalonyl CoA mutase
24
Q

in cis double bonds in beta oxi. Each double bond yields

A

1.5 fewer ATPs than corresponding saturated FA

25
Q

peroxisomal beta oxidation is more __ than mito. beta oxidation
and
will not proceed beyond __?

A

specific
and
c8

26
Q

MCAD Deficiency

A

Medium-chain acyl-CoA dehydrogenase
vomitting lethargy and coma
cause : hypoketotoic hypoglycemia , and dicarboxylic aciduria

27
Q

hypoglycemia?

A

Fasting, decreased Gluconeogensis, increased glucose use

28
Q

dicarboxylic aciduria

A

alter. ox FA

29
Q

ketotoic ?

A

can’t degrade FA

30
Q

MCAD is associated with

A

Reyes syndrome or infeant death syndrome

31
Q

diabetic ketoacidosis causes ?

A
  1. incease glucagon/insulin ratio
  2. increase deg of FA
  3. increase acetyl coa
  4. increase ketonee bodies
  5. incerease ph
32
Q

Abeta-lipoproteinemia….

A

Defective synthesis of B apoproteins…
Formation of chylomicrons & VLDLs are affected…
Can’t transport dietary lipid for storage
Chylomicrons, VLDLs, and LDLs are absent from plasma
neuropathy and red cell formation

33
Q

during fasting/diabetes what happens to fat storage and LPL concentrations

A

they decrease

34
Q

in the well fed state what happens to fat storage and LPL concentrations

A

they increase

35
Q

in the well fed state insulin __ and fat storage __

A

inccrease , decrease

36
Q

in the diabetes/fasting state insulin __ and fat storage __

A

decrease and increase

Biochemistry (9 decks)

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