Insulin Action and Resistance Flashcards

1
Q

What is meant by the fed state?

A

High insulin, low glucagon

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2
Q

What is meant by the fasting state?

A

Hugh glucagon, low insulin

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3
Q

What happens to glucose in the blood stream with respect to the liver in the fed state?

A

It gets taken up into the liver

It is synthesised into glycogen

Excess glucose in the liver is made into VLDL and put back into the circulation

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4
Q

Which body tissues have glucose transporters that are NOT insulin dependant?

Which transporters are these?

What does this mean for these tissues?

A

Brain (GLUT3) and RBC’s (GLUT1)

They will take up glucose all the time

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5
Q

Which glucose transporter is involved in glucose uptake into the liver?

A

GLUT2

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6
Q

Which glucose transporter is involved in glucose uptake into the skeletal muscle and adipose tissue?

A

GLUT4

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7
Q

What happens to glucose in the blood stream with respect to the adipose tissue and skeletal muscle in the fed state?

A

It is taken up by GLUT4 transporters and stored as glycogen (muscle) and triglycerides (adipose tissue)

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8
Q

What happens in the liver in the fasting state?

A

Glucagon stores are broken down into glucose which is released into the blood stream to feed the RBC and Brain

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9
Q

What happens in the adipose tissue in the fasting state?

A

It releases fatty acids, which are used by the muscle as energy supply

The liver also uses these fatty acids to produce ketone bodies which can be used as fuel

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10
Q

Can we convert fatty acids into glucose?

A

No, only into ketones

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11
Q

What happens to proteins from the muscle and lactate from the RBC’s in the fasting state?

A

It goes to the liver to produce glucose to feed the brain

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12
Q

Why do urea levels go up in the fasting state?

A

Urea is made from the nitrogenous breakdown of protein, which occurs in the fasting state

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13
Q

Can the brain use ketone bodies for energy?

A

Yes

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14
Q

What is the T1DM state?

A
No insulin
High glucagon (as this is free running and usually suppressed by insulin)
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15
Q

What happens in T1DM metabolism?

A

Insulin levels non existent
Glucose levels in blood are high
Gluconeogenosis and glycogenolysis still occur, depleting stores
Protein breakdown and fatty acid breakdown occur
Ketone bodies get higher as higher as does blood glucose levels
Glucose and ketone bodies are seen in urine
Ketoacidosis May occur

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16
Q

What type of receptor is the insulin receptor?

What does this mean in terms of its action?

A

Tyrosine kinase receptor

It phosphorylates tyrosine in itself (auto-phosphorylation), then phosphorylates other molecules within the cells such as insulin receptor substrates

17
Q

Which kinases are responsible for:

1) metabolic effects of insulin
2) genetic expression effects of insulin

A

1) PI3-kinase

2) RAS kinase

18
Q

What group of enzymes dephosphorylates structures?

A

Phosphotases

19
Q

Why do people get T2DM?

A

Obesity = more adipose tissues = products = interfere with insulin signalling = ?aetiology - mainly unknown = causes insulin resistance

Adipose tissue expansion also recruiters macrophages which release proinflammatory cytokines which interfere with adiponectin, lectin and the insulin receptor pathway

20
Q

Which type of adipose tissue is mainly implicated in insulin resistance?

A

Visceral

21
Q

What good things does adipose tissue produce?

What do they do?

What happens to them with obesity?

A

Leptin = increases insulin sensitivity and helps with satiety = in obesity body becomes resistant

Adiponectin = increases insulin sensitivity = decreases in synthesis and secretion in obesity