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Flashcards in Integration of Metabolism Deck (35)
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1

What % of our body mass is made up of skeletal muscle

40-50%

2

What % of our resting oxygen consumption is from skeletal muscle

20-30%

3

What % of our insulin-mediated glucose disposal comes from skeletal muscle

75%

4

Prolonged increases in blood glucose can lead to what, causing diabetes

Insulin resistance

5

Insulin resistance will lead to de novo lipogenesis. What does this cause

Increased fat levels

6

Describe the Randle's cycle

an alternating interaction between glucose and FFA metabolism. It explains the inhibition of glucose oxidation by fatty acids

7

Why is glucose oxidation inhibited by FAs- Randle's cycle

A greater amount of fat through the fat oxidation pathway increases acetyl CoA,
which inhibits PDC.
An increase in citrate also inhibits PFK,
which inhibits glycolysis as a whole.

8

What suggests regulation of FA at PFK

Increased plasma FFA via lipid and heparin infusion

9

What suggests regulation of FA at glut-4

A decrease in glucose uptake during moderate intensity

10

Decreased free ADP and AMP levels suggest regulation at what enzyme in glycolysis

Glycogen phosphorylase

11

Why can the Randle's cycle be reversed in the fed state?

Both medium and long chain FFAs can't enter the fat oxidation cycle without the help of carnitine

12

Increasing glucose availability inhibits fat oxidation at which transporter

CPT1

13

To preserve glucose supply to tissues relying on glucose, what stimulates adipose tissue lipolysis + hepatic glucose production?

High insulin/glucose ratio

14

How can CHO intake affect absorption insulin/glucagon ratio

Lower intake = lower ratio

15

What does malonyl-coA do

Inhibits CPT1 and increases glucose flux as a result

16

How are malonyl-coA and the Randle hypothesis linked

As long duration exercise causes no change/increase in Malonyl CoA.. this shows the Randle hypothesis may not be true as this doesn't fit with it

17

What is insulin secreted from the pancreas in response too? (Other than glucose)

Protein + CHO

18

Give the key steps in insulin signalling/Insulin stimulated glucose uptake

1. glucose arrives at the cell
2. insulin released
3. insulin binds to IRS-1
4. Signal transduction cascade
5. glut 4 translocation
6. glucose enters via facilitated diffusion and undergos glycolysis

19

Describe Carnitine

Carnitine mediates the transport of medium/long chain fatty acids across the mitochondrial membranes, facilitating oxidation. It is a cofactor for CPT1, to allow FFA to enter the mitochondrion, by forming acyl-carnitine.

20

what does carnitine act as a buffer for

a buffer for excess access acetyl-coA groups allowing glycolysis to continue

21

Where in the body is 95% of carnitine found

Skeletal muscle

22

How does carnitine feeding alter CHO/fat metabolism and exercise performance

Feeding carnitine doesn’t enter the muscle very quickly- no effect on performance/metabolism

23

Which fuel oxidation does carnitine increase

Fat oxidation- glycogen sparing

24

Define insulin resistance

The reduced responsiveness of skeletal muscle glucose uptake to normal circulating levels of insulin

25

Other than the responsiveness of skeletal muscle to glucose uptake, where can insulin resistance be present?

• Impaired ability of insulin to stimulate glucose oxidation (via PDC)
• Impaired ability of insulin to stimulate microvascular perfusion
• Impaired ability of insulin to stimulate amino acid uptake into muscle cells
• Impaired ability of insulin to inhibit muscle protein breakdown

26

If IRS-1 is inhibited, what process is inhibited

Glut-4 translocation

27

Give one method of measuring insulin resistance

hyperinsulinemic-euglycemic clamp technique

28

What is the hyperinsulinemic-euglycemic clamp technique

maintaining a high insulin level by perfusion, or infusion with insulin at a set rate. It is a way to quantify how sensitive the tissue to insulin

29

True or False: Insulin sensitivity declines naturally over a lifetime.

True

30

Give 3 general causes of Insulin resistance

an increased energy intake, physical inactivity, and obesity