Diabetes Mellitus: Insulin action Flashcards
<p>Which Glucose transporter does insulin stimulate?</p>
<p>GLUT-4</p>
<p>Where are GLUT-4 receptors in the absence of insulin?</p>
<p>In vesicles in the cytoplasm</p>
<p>What happens to GLUT-4 receptors when there is an increase in insulin levels?</p>
<p>They are recruited to the plasma membrane resulting in a 7-fold increase in glucose uptake</p>
<p>Describe the structure of GLUT-4:</p>
<p>Hydrophobic outside, with hydrophilic ring on inside</p>
<p>What is the effect of insulin on protein?</p>
<p>Insulin stops proteolysis and increases the re-sysnthesis of proteins</p>
<p>What is the effect of cortisol on proteins?</p>
<p>Increases proteolysis</p>
<p>What is the effect of insulin on the liver?</p>
<p>Inhibits gluconeogenesis</p>
<p>What is the effect of insulin on adipocytes?</p>
<p>Increases hydrolysis of triglycerides in blood by lipoprotein lipase
Increases formation of triglycerides in adipocytes</p>
<p>What can glycerol be made into in the liver?</p>
<p>Triglycerides
| Glucose</p>
<p>Can the liver make glucose from fatty acids?</p>
<p>Nope</p>
<p>What can the brain use as respiratory substrates?</p>
<p>Glucose
Ketone bodies
Cannot use Fatty acids</p>
<p>How are ketone bodies made and where?</p>
<p>Non-esterified fatty acids broken down into: acetone acetoacetate and 3-hydroxybutyrate in Liver</p>
<p>When blood glucose is too low to support the brain, what happens?</p>
<p>Glucagon stimulates ketone body formation</p>
<p>What is the insulin deficiency test?</p>
<p>Measure levels of ketones and glucose in urine.
| If both high together, insulin deficient </p>
<p>What hormone triggers hepatic glycogenolysis?</p>
<p>Glucagon</p>
<p>What is significant about glucose that enters muscle?</p>
<p>Cannot be removed, must be either respired or stored as glucagon by that muscle</p>
<p>Describe the fasted state:</p>
<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>
<p>Describe the fed state:</p>
<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>
<p>Describe the presentation of T1D:</p>
<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>
<p>Describe insulin induced hypoglycaemia:</p>
<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>
What is dyslipidaemia?
Abnormal amount of lipids in the blood
What are the two pathways effected by insulin?
Metabolic pathway (PI3K-Akt) Mitogenic Pathway (MAPK)
Which pathway does insulin resistance lie in?
Metabolic pathway
What does initial insulin resistance cause?
Compensatory Hyperinsulinaemia, so increased stimulation of the MAPK pathway, so smooth muscle hypertrophy leading to hypertension; reduced ovarian function and abnormal clotting
Describe the presentation of T2D:
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
How should someone with T2D eat?
Controlling of total calories, reducing calories as fats/refined carbohydrates
Increasing calories as complex carbohydrates
Increasing soluble fibre and decreasing sodium
