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

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Flashcards in MCP - Turner - Fatty Acid Storage/Oxidation - 2/23 Deck (24)
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1

What is the function of lipoprotein lipase?

Promotes hydrolysis of TG from chylomicrons and VLDL

2

How does insulin promote glucose uptake into adipocytes?

Increases # of GLUT4 receptors

3

How are NEFAs transported into adipocytes?

FATP1 FA transporters

4

T/F: Uncomplexed long chain NEFAs are toxic.

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

5

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

a glycerol backbone.

6

What is de-esterification, used in fat mobilization?

Release of NEFAs from TGs

7

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

diacylglycerol
monoacylglycerol

*activated by catecholaines and glucagon via phosphorylation

8

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

Adipose triglyceride lipase

9

What are perilipiins?

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.

10

How are NEFA transported in the blood?

Bound to albumin

11

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

oxidized

12

Which two unsaturated FAs are considered essential in the diet?

Linoleic (18:2omega6) "omega6 class"
Linolenic (18:3omega3) "omega3 class"

13

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

True

14

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

thiokinase aka acyl-CoA synthetase

15

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

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.

16

Every NADH is worth how many ATPs?

3

17

Every FADH2 is worth how many ATPs?

2

18

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

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

19

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

Glycolysis: 36 ATP for C6 oxidized
Beta-oxidation - 129 ATP per C16 oxidized (8 ATP/C)

20

What is the role of enoyl-CoA isomerase?

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

Why are ketone bodies only produced in the liver mitochondria?

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

22

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

True

23

Can the liver use ketone bodies for fuel?

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

24

How does uncontrolled type I diabetes cause ketosis?

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