Diabetes Mellitus: Insulin action Flashcards

1
Q

<p>Which Glucose transporter does insulin stimulate?</p>

A

<p>GLUT-4</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

<p>Where are GLUT-4 receptors in the absence of insulin?</p>

A

<p>In vesicles in the cytoplasm</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

<p>What happens to GLUT-4 receptors when there is an increase in insulin levels?</p>

A

<p>They are recruited to the plasma membrane resulting in a 7-fold increase in glucose uptake</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

<p>Describe the structure of GLUT-4:</p>

A

<p>Hydrophobic outside, with hydrophilic ring on inside</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

<p>What is the effect of insulin on protein?</p>

A

<p>Insulin stops proteolysis and increases the re-sysnthesis of proteins</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

<p>What is the effect of cortisol on proteins?</p>

A

<p>Increases proteolysis</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

<p>What is the effect of insulin on the liver?</p>

A

<p>Inhibits gluconeogenesis</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

<p>What is the effect of insulin on adipocytes?</p>

A

<p>Increases hydrolysis of triglycerides in blood by lipoprotein lipase
Increases formation of triglycerides in adipocytes</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

<p>What can glycerol be made into in the liver?</p>

A

<p>Triglycerides

| Glucose</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

<p>Can the liver make glucose from fatty acids?</p>

A

<p>Nope</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

<p>What can the brain use as respiratory substrates?</p>

A

<p>Glucose
Ketone bodies

Cannot use Fatty acids</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

<p>How are ketone bodies made and where?</p>

A
<p>Non-esterified fatty acids broken down into:
acetone
acetoacetate and 
3-hydroxybutyrate 
in Liver</p>
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

<p>When blood glucose is too low to support the brain, what happens?</p>

A

<p>Glucagon stimulates ketone body formation</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

<p>What is the insulin deficiency test?</p>

A

<p>Measure levels of ketones and glucose in urine.

| If both high together, insulin deficient </p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

<p>What hormone triggers hepatic glycogenolysis?</p>

A

<p>Glucagon</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

<p>What is significant about glucose that enters muscle?</p>

A

<p>Cannot be removed, must be either respired or stored as glucagon by that muscle</p>

17
Q

<p>Describe the fasted state:</p>

A

<p>•Low Insulin:Glycogen ratio
•Blood glucose concentration is NORMAL because the change in Insulin:Glucagon ratio maintains a normal blood glucose concentration
•Muscle use lipid
•Brain uses glucose and then, at a later stage, ketone bodies
•INCREASE IN:
-Concentration of NEFA
-Proteolysis
-Lipolysis
-Hepatic Glucose Output (from glycogenolysis and gluconeogensis)
•DECREASE IN:
-Amino Acid Concentration (when prolonged)</p>

18
Q

<p>Describe the fed state:</p>

A
<p>•High Insulin:Glucagon ratio
•Stored insulin is released then you get 2nd phase insulin release
•Stop Hepatic Glucose    Output
•INCREASE IN:
-Glycogen
-Protein Synthesis
-Lipogenesis
•DECREASE IN:
-Gluconeogenesis
-Proteolysis</p>
19
Q

<p>Describe the presentation of T1D:</p>

A

<p>Absolute insulin deficiency leading to:

- Loss of muscle mass due to proteolysis
- Lipolysis
- High Hepatic glucose output, so goes to kidney and not fully reabsorbed; glycosuria and ketonuria</p>

20
Q

<p>Describe insulin induced hypoglycaemia:</p>

A

<p>High concurrent insulin AND glucagon levels, causing glucose top continue entering muscle.
Glucagon will eventually trump insulin, but IM glucagon can be given</p>

21
Q

What is dyslipidaemia?

A

Abnormal amount of lipids in the blood

22
Q

What are the two pathways effected by insulin?

A
Metabolic pathway (PI3K-Akt)
Mitogenic Pathway (MAPK)
23
Q

Which pathway does insulin resistance lie in?

A

Metabolic pathway

24
Q

What does initial insulin resistance cause?

A

Compensatory Hyperinsulinaemia, so increased stimulation of the MAPK pathway, so smooth muscle hypertrophy leading to hypertension; reduced ovarian function and abnormal clotting

25
Q

Describe the presentation of T2D:

A

Insulin resistance with 60-80% obese and dyslipidaemia

Later insulin deficiency with hyperglycaemia

Has less osmotic symptoms yet has complications

Likely to present late with complications unlike T1DM as that is caught earlier

26
Q

How should someone with T2D eat?

A

Controlling of total calories, reducing calories as fats/refined carbohydrates

Increasing calories as complex carbohydrates

Increasing soluble fibre and decreasing sodium