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
