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Flashcards in 3.2-Fed/Fast Cycle Deck (31):
1

Big picture Q: What are the major suppliers for GNG? ALSO where do these come from?

Lactate! (Major one, from Muscle) AAs (Alanine from Muscle, Glutamate from diet, and Glutamine from diet), Glycerol (from Adipose)

2

About how many g of glucose does the brain consume per day? What percentage of total body glucose is this?

120g/day...60% of body's glucose

3

Why doesn't the CNS use fat for fuel?

It cannot cross the blood/brain barrier

4

What are the three major fuels for muscle?

glucose, fatty acids, ketone bodies

5

What is the main fuel for muscle during exertion? What about rest?

Glucose (glycolysis not CAC and beyond) during exertion and rest it uses FA's

6

What is the heart's main fuel? What are its two alternatives?

Fatty Acids, with ketone bodies and lactate as alternatives

7

Why is the amount of glucose in an adipose cell a major factor in determining whether FAs are released to the blood?

HAS TO DO WITH G-3-P: Low glucose=low G-3-P=get FAs out, High glucose = high G-3-P, time to store

8

What is the task of the kidney that requires a lot of energy?

Reabsorption of nutrients from blood

9

What main metabolic task does the kidney perform under starvation circumstances?

GNG, can be 1/2 of all blood glucose!!

10

About how much glucose is removed from blood by the liver?

About 2/3!!

11

What three things does the liver synthesize when there is an abundance of glucose around? ALSO what metabolic pathway does it perform to get NADPH?

Fatty Acids, Cholesterol, and Bile Salts....PPPathway!

12

What molecule prevents long chain FAs from entering the matrix?

Malonyl CoA. (wants to MAKE fat not break it down!)

13

What are FAs converted to in a starvation state?

Ketone Bodies! Remember, we can not make Glucose from acetyl-CoA!!

14

What is the primary use of dietary AAs that go to the liveR?

Protein Synthesis! Not necessarily catabolism

15

Which AAs have to be catabolised in the muscle because the liver cannot do it?

Leucine, IsoLeucine, Valine.. Because they are all branched!

16

Which product of ketone body formation cannot be used by the liver? (What a nice organ, it sends it to the brain :)

Ace-to-ace-tate

17

What 2 processes does the liver perform when entering our early fasting state?

Get glucose into the blood! Glycogenolysis and GNG!

18

What is the phenomena happening after 2 days of starvation and GNG starts to drop in production?

Ketone bodies are now being produced and the brain can run off those

19

What is the key pathway as we begin to go into prolonged starvation?

GNG

20

What is the very friendly thing that muscle does to help the body out in prolonged starvation?

Muscle initially loves using Ketone bodies, but going into prolonged starvation, muscle stops using them and gives them to the brain. This puts less strain on the liver to stop having to to GNG! (sparing the protein precursors)

21

During prolonged fasting: does the utilization of ketone bodies increase or decrease?

Decrease

22

During prolonged fasting: does utilization of ketone bodies in the brain increase or decrease?

Increase

23

During prolonged fasting: does the liver increase or decrease GNG?

Decrease (its expensive!)

24

During prolonged fasting: does muscle increase or decrease protein degradation?

Decrease (hold on to what you can!)

25

During prolonged fasting: does the liver increase or decrease production of urea?

Decrease (it costs a lot of ATP!)

26

What happens to glucose levels in the blood after 4 days of starvation and beyond?

It levels out and stays constant at ~3 mM...WEIRD?

27

What does a decrease in Urea production during starvation reflect?

Decreased breakdown of muscle protein

28

What is special about how the liver interacts with glucose after a "re-fed" state? Does it do GNG in this state?

The liver does not automatically absorb the glucose, but leaves it for the peripheral tissues...YES still GNGs

29

What is our MASTER SWITCH in metabolism? What does it do to change things?

AMPK! (AMp-activated Proetin Kinase)...When high AMP ratio, it shuts down processes that use ATP and promotes processes that build ATP

30

What are the two molecules that trigger AMPK? The first one is so obvious I will kill you if you get it wrong..

High AMP/ATP ratio & High Creatine/Phosphocreatine ratio

31

HOW does AMPK shut down ATP using processes and promote ATP creating processes?

AMPK phosphorylates rate-limiting enzymes! (In BOTH energy producing and energy using pathways..)