lipid metabolism Flashcards

1
Q

what is the starting product for fatty acid synthesis?

A

citrate (accumulates in the fed state)

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2
Q

where is fatty acid synthesis occurring?

A

cytoplasm

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3
Q

how does citrate move into the cytoplasm?

A

citrate shuttle

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4
Q

how is citrate converted to acetyl-CoA?

A

ATP citrate lyase

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5
Q

how is acetyl coA converted to malonyl CoA? required cofactor?

A

acetyl-CoA carboxylase (RLS), biotin

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6
Q

only ___ fatty acids can be made from malignly coA

A

even chain

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7
Q

where does fatty acid catabolism occur?

A

in the mitochondria

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8
Q

how are fatty acids transported into mitochondria?

A

1) fatty acid coA synthetase converts to acyl-CoA

2) acyl-CoA enters mitochondria via carnitine shuttle

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9
Q

what inhibits the carnitine shuttle?

A

malonyl-CoA (preventing degradation of newly synthesized FAs)

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10
Q

what are the 2 possible fates of B-oxidation products?

A

ketone bodies

TCA cycle

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11
Q

what is the effect carnitine deficiency?

A

decreased carnitine shuttle leads to inability to move LCFA into mitochondria

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12
Q

symptoms of carnitine deficiency (3)

A

weakness
hypotonia
hypokeotoic hypoglycemia

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13
Q

2 substances synthesized from HMG-CoA

A
cholesterol
ketone bodies (acetoacetate)
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14
Q

what is the only energy source of RBCs?

A

glucose

cannot use ketone bodies (lack mitochondria)

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15
Q

ketone bodies can be used for energy because they are converted to

A

2 acetyl-CoA

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16
Q

what is the rate limiting enzyme in ketone body synthesis?

A

HMG CoA synthase

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17
Q

which ketone body is preferred by the brain?

A

b-hydroxybutarate

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18
Q

what gives breath a fruity odor?

A

acetone

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19
Q

where are ketone bodies produced?

A

made in the liver, although the liver lacks the enzymes needed to use them

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20
Q

reaction by HMG-CoA reductase

A

HMG-COA to mevalonate

21
Q

function of LCAT

A

esterifies cholesterol, which allows it to be stored in vesicles (important for transport throughout the body), like HDL

22
Q

pancreatic lipase

A

degrades dietary triglycerides to 2 free FA and monoacylglycerol- allows for absorption into enterocyte

23
Q

lipoprotein lipase location, function

A

endothelium

degrades triglycerides circulating in chylomicrons, VLDL

24
Q

hepatic lipase location, function

A

liver

degrades triglycerides in IDL to form LDL

25
hormone sensitive lipase location, function
intracellular | degrades triglycerides in adipocytes
26
CETP
mediates transfer of cholesterol to other lipoproteins
27
Apo E
mediates remnant uptake into liver
28
ApoA-I
activates LCAT | found only on HDL
29
ApoC-II
cofactor for lipoprotein lipase
30
apoB-48
mediates chylomicron assembly and secretion
31
apoB100
binds LDL receptor, mediates release of VLDL from liver, involved in receptor-mediated endocytosis of LDL by cells
32
role of chylomicrons
deliver dietary TGs to peripheral tissue
33
role of VLDL
deliver TGs from liver to peripheral tissue
34
role of LDL
delivers hepatic cholesterol to peripheral tissues
35
why does LDL contain mostly cholesterol?
VLDL was acted on by lipoprotein lipase to deliver triglycerides to tissue, leaving cholesterol
36
role of HDL
carries cholesterol from the periphery to the liver
37
type I hyperchylomicronemia increases (3)
chylomicrons, triglycerides, cholesterol
38
2 causes of type I hyperchylomicronemia
AR defect of lipoprotein lipase or Apo C-II
39
symptoms of type I hyperchylomicronemia
pancreatitis, xanthomas | *no increased risk for atherosclerosis
40
type IIa familial hypercholesterolemia increases (2)
LDL, cholesterol
41
cause of type IIa familial hypercholesterolemia
AD decreased or absent LDL receptors
42
symptoms of type IIa hypercholesterolemia
atherosclerosis, tendinous xanthomas, corneal arcus
43
type III dysbetalipoproteinemia is caused by:
defects in ApoE, leads to increased chylomicron remnants in the circulation
44
type IV hypertriglyceridemia increases (2)
VLDL, triglycerides
45
type IV hypertriglyceridemia is caused by:
AD hepatic overproduction of VLDL, absent ApoA-V
46
symptoms of type IV hypertriglycermidemia
pancreatitis
47
what causes abetalipoproteinemia?
AR lack of B48 and B100 due to mutation in MTP gene leads to decreased chylomicron and VLDL synthesis and secretion, fat cannot be absorbed and instead, accumulates in enterocytes
48
symptoms of abetalipoproteinemia (4)
steatorrhea, acanthocytosis, ataxia, night blindness