Integration of Metabolism Flashcards

(35 cards)

1
Q

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

A

40-50%

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2
Q

What % of our resting oxygen consumption is from skeletal muscle

A

20-30%

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3
Q

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

A

75%

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4
Q

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

A

Insulin resistance

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5
Q

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

A

Increased fat levels

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6
Q

Describe the Randle’s cycle

A

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

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7
Q

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

A

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.

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8
Q

What suggests regulation of FA at PFK

A

Increased plasma FFA via lipid and heparin infusion

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9
Q

What suggests regulation of FA at glut-4

A

A decrease in glucose uptake during moderate intensity

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10
Q

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

A

Glycogen phosphorylase

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11
Q

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

A

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

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12
Q

Increasing glucose availability inhibits fat oxidation at which transporter

A

CPT1

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13
Q

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

A

High insulin/glucose ratio

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14
Q

How can CHO intake affect absorption insulin/glucagon ratio

A

Lower intake = lower ratio

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15
Q

What does malonyl-coA do

A

Inhibits CPT1 and increases glucose flux as a result

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16
Q

How are malonyl-coA and the Randle hypothesis linked

A

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
Q

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

A

Protein + CHO

18
Q

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

A
  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
Q

Describe Carnitine

A

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
Q

what does carnitine act as a buffer for

A

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

21
Q

Where in the body is 95% of carnitine found

A

Skeletal muscle

22
Q

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

A

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

23
Q

Which fuel oxidation does carnitine increase

A

Fat oxidation- glycogen sparing

24
Q

Define insulin resistance

A

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
31
What disease does insulin resistance lead too?
Type 2 diabetes
32
What is metabolic inflexibility?
Switching between substrates. Where we are less good at regulating fat and stay hyperglycaemic.
33
What is the lipid overspill theory?
An individual’s capacity to store lipids in adipose tissue has a set maximal limit. When this is exceeded, excess lipids spill into plasma, elevating plasma FFA and triglyceride levels.
34
Other than glut-4, what else can directly effect fat oxidation via CPT1
AMPK
35
Give 2 methods to treat insulin resistance
1. Weight loss via calorie restriction 2. Endurance exercise training 3. Resistance training 4. Pharmacological to a. Increase insulin sensitivity b. Or mimic insulin