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

Question 1

What is the function of lipoprotein lipase?

Answer 1

Promotes hydrolysis of TG from chylomicrons and VLDL

Question 2

How does insulin promote glucose uptake into adipocytes?

Answer 2

Increases # of GLUT4 receptors

Question 3

How are NEFAs transported into adipocytes?

Answer 3

FATP1 FA transporters

Question 4

T/F: Uncomplexed long chain NEFAs are toxic.

Answer 4

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

Question 5

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

Answer 5

a glycerol backbone.

Question 6

What is de-esterification, used in fat mobilization?

Answer 6

Release of NEFAs from TGs

Question 7

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

Answer 7

diacylglycerol
monoacylglycerol

*activated by catecholaines and glucagon via phosphorylation

Question 8

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

Answer 8

Adipose triglyceride lipase

Question 9

What are perilipiins?

Answer 9

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.

Question 10

How are NEFA transported in the blood?

Answer 10

Bound to albumin

Question 11

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

Answer 11

oxidized

Question 12

Which two unsaturated FAs are considered essential in the diet?

Answer 12

Linoleic (18:2omega6) “omega6 class”

Linolenic (18:3omega3) “omega3 class”

Question 13

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

Answer 13

True

Question 14

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

Answer 14

thiokinase aka acyl-CoA synthetase

Question 15

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

Answer 15

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.

Question 16

Every NADH is worth how many ATPs?

Answer 16

3

Question 17

Every FADH2 is worth how many ATPs?

Answer 17

2

Question 18

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

Answer 18

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

Question 19

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

Answer 19

Glycolysis: 36 ATP for C6 oxidized

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

Question 20

What is the role of enoyl-CoA isomerase?

Answer 20

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.

Question 21

Why are ketone bodies only produced in the liver mitochondria?

Answer 21

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

Question 22

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

Answer 22

True

Question 23

Can the liver use ketone bodies for fuel?

Answer 23

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

Question 24

How does uncontrolled type I diabetes cause ketosis?

Answer 24

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