Lipid Metabolism Part II Lipoprotein Metabolism Flashcards

1
Q

what is mean by postabsorptive state?

A

means fatty acids can be released from adipose tissue to be used for energy.

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2
Q

The fall in insulin activates a ____________ that hydrolyzes triglycerides, yielding ______________.

A

hormone-sensitive triacylglycerol lipase (HSL) ,
fatty acids and glycerol.

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3
Q

Epinephrine and cortisol. also _____________.

A

activate HSL .

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4
Q

Free fatty acids are transported through the blood in association with___________

A

serum albumin.

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5
Q

what will be picked up by liver and converted to what for gluconeogenesis?

A

Glycerol may be picked by liver, converted to dihydroxyacetone phosphate (DHAP)

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6
Q

fatty acids are oxidized into tissues including what and by which pathway?

A

liver, muscle, and adipose tissue, by β-oxidation pathway.

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7
Q

What can NOT use fatty acids and so continue to rely on glucose during what time?

A

Erythrocytes and brain, during normal periods of fasting.

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8
Q

Erythrocytes lack ____________, and fatty acids do not cross the______________ efficiently.

A

mitochondria, blood–brain barrier.

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9
Q

what all diffuse freely into mitochondria to be oxidized.

A

short-chain fatty acids and medium-chain fatty acids.

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10
Q

long-chain fatty acids must be ____________& transported into the mitochondrion by a _______________ to be oxidized.

A

activated, carnitine shuttle

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11
Q

very long-chain fatty acids enter _______________
via an unknown mechanism for oxidation.

A

enter peroxisomes

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12
Q

_____________on the outer mitochondrial membrane, activates the fatty acids by attaching CoA.

A

Fatty acyl-CoA synthetase

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13
Q

The fatty acyl portion is then transferred onto carnitine by _________________for transport into the mitochondria.

A

carnitine acyltransferase-1 (CAT-1).

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14
Q

what is shuttled across the inner membrane.

A

Fatty acylcarnitine

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15
Q

Carnitine acyltransferase-2 (CAT-2)/ carnitine palmitoyl transferase-2 (CPT-2) transfers the ______________ back to ___________.

A

fatty acyl group, a CoA .

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16
Q

Carnitine acyltransferase-1 is inhibited by _____________.

A

malonyl-CoA .

17
Q

Carnitine acyltransferase-1 prevents newly synthesized fatty acids from entering the ______________.

A

mitochondria.

18
Q

Insulin indirectly inhibits β-oxidation by activating ____________ and increasing the ____________ concentration in the cytoplasm which inhibits_____________.

A

acetyl-CoA carboxylase, malonyl-CoA, Carnitine acyltransferase.

19
Q

Carnitine acyltransferase-1 and -2 (CAT-1 and CAT-2) are also called as?

A

carnitine palmitoyl transferase-1 and -2 (CPT-1 and CPT-2).

20
Q

what reverses the process of fatty acid synthesis by oxidizing?

A

β-oxidation.

21
Q

β-oxidation after oxidizing it releases units of _______________ and what is the pathway of it?

A

acetyl-CoA, repetition of 4 steps.

22
Q

Each 4-step cycle releases one _________and reduces NAD and FAD producing___________.

A

acetyl-CoA, NADH and FADH2

23
Q

FADH2 and NADH are oxidized in the __________ providing ATP.

A

electron transport chain.

24
Q

what cycle does muscle and adipose tissue, the acetyl-CoA enters to?

A

citric acid cycle.

25
Q

in liver ATP used for what?

A

Gluconeogenesis.

26
Q

By activating what does acetyl-CoA stimulates gluconeogenesis?

A

Pyruvate carboxylase.

27
Q

In a ___________ state, the liver produces more acetyl-CoA from β-oxidation than is used in the citric acid cycle

A

fasting state

28
Q

the acetyl-CoA is used to synthesize __________ that are released into the blood for other tissues.

A

ketone bodies.

29
Q

What are the two most common genetic deficiencies affecting fatty acids oxidation ?

A

1.Medium chain acyl-CoA dehydrogenase (MCAD) deficiency. (it’s in liver.)
2.Myopathic carnitine acyltransferase (CAT/CPT) deficiency. (it’s in muscle.)

30
Q

In MCAD______________ should be strongly associated with a block in hepatic β-oxidation.

A

Non-ketortic hypoglycemia .

31
Q

In MCAD______________ should be strongly associated with a block in hepatic β-oxidation.

A

Non-ketortic hypoglycemia.

32
Q

At what period hypoglycemia can become profound due to lack of ATP to support gluconeogenesis.

A

During fasting.