M1-C1-L77 --> Lipid Metabolism

Front 1

In the fasted state, what happens with glucagon?

Back 1

Goes up.

Front 2

In the fasted state, what happens with epinephrine?

Back 2

Goes up.

Front 3

In the fasted state what happens with insulin?

Back 3

Decreases

Front 4

Triglyceride breakdown requires the stimulation from what molecules?

Back 4

Glucagon
Epinephrine

Front 5

What are the generalized sequence of events that occurs with triglyceride breakdown?

Back 5

1. Intracellular cAMP INCREASES and ACTIVATES protein kinase A.
2. Phosphorylation and activation of hormone sensitive lipase.
3. Degradation of triglyceride to free fatty acids and glycerol.

Front 6

Post degradation of triglycerides, what happens to FFA and glycerol in the fasted state?

Back 6

Both will diffuse into blood, where FFA will bind to serum albumin. Glycerol is soluble.

Front 7

In the liver, glucagon and epinephrine stimulate WHAT to form WHAT products for what process?

Back 7

Beta Oxidation
Ketones and Glycerol
Gluconeogenesis

Front 8

What must happen for hormone sensitive lipase to act?

Back 8

Phosphorylation of perilipin

Front 9

What is perilipin?

Back 9

Protein that coats the lipid droplets in adipocytes

Front 10

What happens to the majority of the FFA that are mobilized from adipocytes to be taken up by the liver?

Back 10

In the liver, 60% of FFA is repackaged into lipoproteins and sent back to the adipocytes

Front 11

Glycerol

Back 11

What is this?

Front 12

Addition of each fatty acid on a glycerol requires what kind of energy expenditure?

Back 12

Two high energy bonds (total of 6 ATP)

Front 13

T/F - In the fasted state, adipose release just enough FFA for metabolism.

Back 13

F - In the fasted state, adipose releases more FFA than is needed for metabolism.

Front 14

Describe the actions oof the liver with extra FFA in the fasted state. x 3

Back 14

1. Liver RE-ESTERIFIES the fatty acids into triglycerides.
2. PACKAGES the lipid into lipid protein.
3. SECRETES it into bloodstream.

Front 15

Repackaging FFA ensures what two things?

Back 15

1. Adequate energy supply
2. Homeostasis of serum lipids in blood

Front 16

Describe the steps in fatty acid transport to mitochondria. x 4

Back 16

1. Formation of fatty acy-CoA.
2. Transfer to carnitine to form fatty acyl-carnitine
3. Facilitated diffusion via acyl-carnitine/carnitine transporter.
4. Transfer back to CoA inside mitochondria.

Front 17

Where would you find Carnitine Acyltransferase I?

Back 17

On the cytoplasmic face of mitochondria.

Front 18

Where would you find Carnitine Acyltransferase II?

Back 18

Inside the mitochondria.

Front 19

What is the overall point in transferring fatty acid to mitochondria?

Back 19

To degrade the long fatty acyl-CoA in to Acetyl CoA. Then, feed Acetyl-CoA into the TCA and make ATP in ETC

Front 20

Usually, Beta oxidation of 1 saturated FFA molecule will produce how many Acetyl-CoA's?

Back 20

Eight

Front 21

Usually, Beta oxidation of 1 saturated FFA molecule will lead to how many CO2's?

Back 21

16 CO2

Front 22

Usually, Beta oxidation of 1 saturated FFA molecule will lead to how many electrons?

Back 22

64 e-

Front 23

What is the major point of beta oxidation?

Back 23

Fatty acids get cleaved to make Acetyl-CoA

Front 24

What is needed for beta oxidation of monoUNSATURATED fatty acid?

Back 24

An isomerase to convert the cis bond to trans.

Front 25

What is needed for beta oxidation of polyUNSATURATED fatty acid?

Back 25

Need a reductase and an isomerase.

Front 26

"When life gives you propionyl-CoA, make".....what?

Back 26

A TCA intermediate (Succinyl CoA)

Front 27

When do you get the three carbon molecule, propionyl CoA?

Back 27

It is the final product in odd-chain fatty acids.

Front 28

How does biotin play a role in odd chain FA beta oxidation?

Back 28

Takes propionyl-CoA and converts it a four carbon intermediate via carboxylation.

Front 29

Under low glucose levels, the brain uses what for food?

Back 29

ketones

Front 30

Which ketone is responsible for bad breath?

Back 30

acetone

Front 31

Ketones are produced from what molecule and where specifically?

Back 31

Acetyl CoA

Hepatocyte mitochondria

Front 32

Describe the general steps in ketone formation in the liver during a fasted state.

Back 32

1. Gluconeogenesis removes oxaloacetate from TCA.
2. Oxaloacetate removal SLOWS down TCA causing accumulation of acetyl-CoA.
3. Acetyl-CoA is then used to make ketones.

Front 33

Loss of insulin in IDDM patients, is due to a loss of what and where?

Back 33

Beta cells in the pancreas.

Front 34

Accumulation of ketones in blood can lead to what?

Back 34

ketoacidosis

Front 35

Ketoacidosis can alter what?

Back 35

Heme functions

Oxygen transport

Front 36

What are the presentations of Carnitine deficiency? x 4

Back 36

1. Hypoketotic Hypoglycemic Encephalopathy.
2. Cardiomyopathy
3. Myopathy
4. GI Dysmotility

Front 37

What parts are effected by Carnitine deficiency? x 3

Back 37

1. CNS
2. Skeletal muscle
3. Cardiac muscle

Front 38

B12 Deficiency causes an accumulation of what molecules? x2

Back 38

Methylmalonyl-CoA
Homocyteine
5-MethylTHF

Front 39

B12 deficiency can cause the same kind of anemia as what other disorders? x2

Back 39

1. Oroticaciduria I
2. Oroticaciduria II

Front 40

Acyl CoA Dehydrogenase deficiency affects what enzymes? x3 from worst symptoms to least.

Back 40

1. VLCAD (Very Long Chain Acyl CoA Dehydrogenase)
2. MCAD (Medium Chain Acyl CoA Dehydrogenase)
3. SCAD (Short Chain Acyl CoA Dehydrogenase)