16. Adipocytokines: Is Adipose Tissue Passive or Active Flashcards

1
Q

what does leptin cause?

A

Insulin resistance

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2
Q

What is adiponectin?

A

an Insulin sensitizer

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3
Q

if you oversupply too much triglyceride on a regular basis into the adipose tissue will cause what?

A

cytokines will be released that will attract more white blood cells which will cause inflammatory. Over-supply of fat will lead to these pro-inflammatory cytokine profiles.

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4
Q

what are the mechanisms that are thought to account for insulin resistance in obese individuals?

A

An increase in fat derivatives and the insulin signalling cascade will be blocked as a result.

Resistin high levels

Lack of adiponectin

high levels in leptin

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5
Q

What happens to the insulin signalling cascade in obese individuals?

A

In a healthy individual this happens….

  • Insulin receptor on the membrane. Insulin attaches to outside of the insulin receptor so that the receptor exposes tyrosine to auto-phosphorylate.
  • IRS-1 can dock on the receptor and auto phosphorylate. This then converts PIP2 to PIP3 to lead to switch on other proteins which lead to the GLUT4 vesicle to move to the cell membrane.

In obese people if you over supply fat to the cell, fat derivatives will begin to increase. You start to see serine phosphorylation in the cell which will block the tyrosine - therefore if insulin comes to the cell the tyrosine will not be phosphorylated thus the cascade will not begin for glucose to be taken up into the cell

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6
Q

What effect does Resistin (an adipocytokine) have on insulin resistance and how can if effects be reversed?

A

Resistin is released front he adipocytes and inhibits the effect insulin has on glucose uptake.

Treatment with anti-Resistin lgl significantly improves insulin sensitivity

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7
Q

If you get people to lose weight, what effect does this have of their adipocytokines?

A

Leptin goes down
Resistin goes down
adiponectin goes up

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8
Q

How does adiponectin increase fat oxidation in the muscle?

A

it attaches to its receptor to activate the phosphorylation of AMPK to deactivate ACC (acetyl-CoA carboxylase) so that malonyl-CoA goes down to prevent fat accumulating.

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