MCP - Turner - Fatty Acid Storage/Oxidation - 2/23 Flashcards

1
Q

What is the function of lipoprotein lipase?

A

Promotes hydrolysis of TG from chylomicrons and VLDL

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2
Q

How does insulin promote glucose uptake into adipocytes?

A

Increases # of GLUT4 receptors

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3
Q

How are NEFAs transported into adipocytes?

A

FATP1 FA transporters

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4
Q

T/F: Uncomplexed long chain NEFAs are toxic.

A

True, that is why when they are transported into the cell, they immediately become bound to adipocyte lipid binding protein

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5
Q

By combined action of thiokinase and acyl transferases, NEFAs are esterified to ______

A

a glycerol backbone.

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6
Q

What is de-esterification, used in fat mobilization?

A

Release of NEFAs from TGs

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7
Q

Hormone-sensitive lipase is one of the best studied esterases. It is known to preferentially release fatty acids from what structures?

A

diacylglycerol
monoacylglycerol

*activated by catecholaines and glucagon via phosphorylation

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8
Q

What is the rate-limiting enzyme, involved in step 1 in hydrolysis (formation of diacylglycerol from TG)?

A

Adipose triglyceride lipase

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9
Q

What are perilipiins?

A

Peripilipins are interspersed proteins in the peripheral fat of lipid droplets and in their non-phosphorylated state can protect TGs from HSL. Hormones like glucagon resultin the phosphorylation of perilipins, which disrupts the sheet, allowing easier access to TGs by HSL.

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10
Q

How are NEFA transported in the blood?

A

Bound to albumin

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11
Q

FA are removed from the blood by various tissues (not the brain) and ___ to yield ATP

A

oxidized

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12
Q

Which two unsaturated FAs are considered essential in the diet?

A

Linoleic (18:2omega6) “omega6 class”

Linolenic (18:3omega3) “omega3 class”

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13
Q

T/F: A FA of one class, for example omega-7, cannot be converted to another class by humans.

A

True

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14
Q

Activation of FA is an energy-dependent step catalyzed by:

A

thiokinase aka acyl-CoA synthetase

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15
Q

Why is carnitine palmitoyl transferase I (CPTI) inhibited by malonyl-CoA?

A

Bc malonyl-CoA is the product of the first committed step in FA biosynthesis. By inhibiting CPTI, you are not making and degrading FA at the same time.

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16
Q

Every NADH is worth how many ATPs?

A

3

17
Q

Every FADH2 is worth how many ATPs?

A

2

18
Q

What is MCAD, medium-chain acyl-CoA dehydrogenase deficiency?

A

MCAD deficiency
build up of octanoylcarnitine (toxic?)
rapid progression if child becomes hypoglycemic

19
Q

Compare beta-oxidation to glycolysis in terms of energy yield.

A

Glycolysis: 36 ATP for C6 oxidized

Beta-oxidation - 129 ATP per C16 oxidized (8 ATP/C)

20
Q

What is the role of enoyl-CoA isomerase?

A

Moves a beta-gamma double bond to an alpha-beta position so that beta-oxidation can occur

2,4-dienoyl-CoA reductase takes care of moving a gamma-delta double bond to beta-gamma, where enoyl-CoA isomerase can move it again to alpha-beta.

21
Q

Why are ketone bodies only produced in the liver mitochondria?

A

Non-liver cells do not have a critical enzyme for the reactions, HMG-CoA lyase

22
Q

T/F: Acetoacetate and beta-hydroxybutyrate can be used as fuel by the brain.

A

True

23
Q

Can the liver use ketone bodies for fuel?

A

No, it doesn’t have the correct enzyme, succinyl-CoA transferase or 3-ketoacyl-CoA transferase

24
Q

How does uncontrolled type I diabetes cause ketosis?

A

No insulin –> no breaks on lipolysis –> max production of NEFAs –> NEFAs go to liver –> liver tries to export NEFAs as LDLs but can’t do all of them –> excess FA goes through beta-oxidation –> extra acetyl-CoA makes ketone bodies –> kidneys cannot excrete ketone bodies