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Bio regulatory systems 2 > diabetes mellitus > Flashcards

diabetes mellitus Flashcards

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1
Q

What are the different actions of insulin?

A
  • decrease HGO
  • Increase muscle uptake
  • Decrease proteolysis
  • decrease lipolysis
  • decrease ketogenesis
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2
Q

What is GLUT 4?

A

Glucose transporter found in muscle cells(myocytes) and fat cells(adipocytes)

  • Highly insulin responsive
  • recruited and enhanced by insulin when glucose in the blood rises
  • Increase thew uptake of glucose 7 fold
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3
Q

What is the structure of GLUT 4 transporters?

A
  • Hydrophobic outer chains
  • hydrophilic inner chains
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4
Q

What is the effect of insulin on muscle cells in the fed state?

A
  • In the fed state(once you have eaten) insulin inhibits the breakdown of protein(protolysis)
  • reduces the oxidation of amino acids(the product of protolysis) -stimulates the conversion of amino acid to protein (increase protein synthesis)
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5
Q

What hormones effect muscle cells in the fasting state?

A

-Cortisol-increases protein breakdown to release amino acids that can then be released by the muscle

-Growth Hormone and IGF-1-stimulates protein synthesis

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6
Q

What is the name of amino acids released from the muscle cells during fasting state?

A

-Gluconogenic -means they can be taken up by the liver and used in gluconeogenesis to produce glucose that can then be released from the liver

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7
Q

What are the cells of the liver called?

A

Hepatocyes

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8
Q

Name 2 gluconogenic amino acids?

A

Pyruvate, lactate

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9
Q

what helps the liver take up amino acids?

A

Glucagon transporters

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10
Q

What is the effect of insulin on the liver in the fed state?

A
  • Increase protein synthesis as amino acids are used and stored as proteins
  • Inhibits gluconeogenesis
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11
Q

What hormones have effect on the liver in fasting state?

A

-Glucagon and cortisol-increase gluconeogenesis to increase hepatic glucose output

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12
Q

What are the 3 main fuel stores and how long do they last?

A

Carbs(from muscle and liver)- short term energy fuel, used up within 16 hours when fasting

Protein- makes up 20% of fuel stores in the body but ideally we don’t want to break this down as muscle is very important in the body, this will be depleted within 15 days when fasting

Fat- 30-40% of fuel in body, biggest energy source after carbs, can live in fasting state for 30-40 days in theory

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13
Q

How are fats stored?

A

1-eat =triglycerides increase in the blood

2- triglycerides are broken down into glycerol and non esterified fatty acids via enzyme LIPO PROTEIN LIPASE(LPL) in blood vessel inner membrane and are taken up into fat cells. This process is activated by the influx of insulin

4- in the fed state insulin increases glucose uptake into the fat cell

5- Insulin converts glycerol and non esterified fatty acids(NEFA) into triglycerides for storage

6- In the fed state insulin inhibits the breakdown of triglycerides in the fat cell because energy does not need to be released

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14
Q

How are fats released for fuel?

A

1- in fasting state Growth hormone and cortisol breaks down triglycerides into NEFA and Glycerol which is then released form the fat cell

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15
Q

What is hepato-portal circulation?

A

heart->GI system(picks up nutrients here)-> Liver (nutriends are processed and stored) Insulin from the pancreas is released straight into this circulation to help it act quickly

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16
Q

What happens to glycerol released from fat cells ?

A

1- Glycerol taken up by the liver via glycerol 3 phosphate transporter 2- If its not needed it can be stored as triglycerides within the liver 3- If you are in fasting state the glycerol is converted to glucose via gluconeogenesis=increase hepatic glucose output

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17
Q

How much of your hepatic glucose output is produced from hepatic gluconeogenesis?

A

25% after 10 hour fast

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18
Q

What fuel source is used by your brain?

A

Glucose-preferred source Ketone bodies Can’t uses fatty acids

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19
Q

What happens to NEFA released from fat cells?

A

1- taken up by the liver via transporter

2-converted into Fatty Acyl CoA

3- In the fed state, INSULIN is high and prevents the Fatty Acyl CoA being broken down into ketone bodies

4-If are in the fasting state you have higher levels of GLUCAGON, causes the breakdown to produce ketone bodies

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20
Q

If you have ketone body production what does this tell you insulin levels in the blood?

A

Insulin levels must be low as insulin prevents the breakdown of fatty Acyl CoA to ketone bodies

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21
Q

When is the production of ketone bodies abnormal ?

A

when you have high glucose levels- this indicates that there must be insulin deficiency as if there is low levels of insulin glucose is not been taken up by the cells and therefore production of ketone bodies is stimulated

22
Q

describe Hepatic glycogenolysis?

A

glycogen->glucose in liver

1-Glucose enters the liver via GLUT2 transporters

2- insulin increases conversion of glucose to glycogen in the liver

3-When in the fasting state glucagon causes glycogen to be broken down into glucose which is them released

23
Q

Where do muscle cells get there fuel from?

A

Fed state- insulin causes glucose to be taken up by the muscle cells. If muscle cell doesnt need glucose at this time then the glucose is converted into glycogen to be used later Fasting state-NEFA taken up by the muscle cells and oxidised to be a source of energy

24
Q

Which hormones prevent the uptake of glucose into the muscle cells?

A

Glucagon Growth hormone happens when you are in the fasted state as blood sugar levels are low

25
Q

what is the difference between glycogen in the liver and in the muscle?

A

muscle-glucose can not be released from muscle, the glucose can only be used by that muscle cell Liver-can be converted to glucose and released form the liver

26
Q

summarise what happens when you are in the fasted state?

A
  • low insulin in blood
  • glucose levels maintained at 3.0-5.5 mmol/l
  • NEFA go up (as fat broken down for energy)
  • amino acid go down if there is a prolonged fast
  • Protolyisis increas
  • increase lipolysis
  • increase HGO from glycogen stores in the liver and gluconeogenesis(happens in the liver)
  • Muscle use lipids
  • Brain uses glucose and the later ketones
  • increase in ketogenesis when the fast is prolonged
27
Q

What happens to your insulin levels when you fast?

A

go down: -this increase proteinolysis -increased hepatic glucose output through the breakdown of glycogen and gluconeognesis -increased lipolysis

28
Q

What happens when you are in the fed state?

A

-stored insulin releases then 2nd phase insulin release (slower) -High insulin to glucagon levels -stop HGO (hepatic glucose output) -increased glycogen -decreased gluconeogenesis -increased protein synthesis -decreased proteolysis -increased lipogenesis

29
Q

What happens to insulin levels in response to feeding?

A

go up: -this increases protein synthesis as you have amino acids from food -stops hepatic glucose output as you get glucose from food so glycogen isnt broken down -increased lipogenesis due to increase in triglycerides from food

30
Q

What tests can you do to diagnose diabetes mellitus?

A

fasting glucose test-done first thing in the morning (more than 7.0mmol/L indicates diabetes) Random glucose test-done any point during the day(more than 11.1mmol/L indicates diabetes) Oral glucose tolerance test-in the morning when you are in fasting state you have a glucose test done then you are given 75g of oral glucose and then another blood glucose test is done after 2 hours(takes long time so kinda impractical) HbA1c- used commonly gives the average glucose for the last 3 months, based on haemoglobin turnover (more than 48mmol/mol indicates diabetes) To properly diagnose you needs a minimum of 2 positive tests or 1 postive test and osmotic symptoms(passing lots of urine, feeling thirsty, needing to pee lots during the night, losing weight)

31
Q

What is type 1 diabetes?

A

Autoimmune condition where your own body produces antibodies that attack the insulin secreting cells in the pancreas so body is unable to produce ANY INSULIN

32
Q

Waht is the pathophysiology of type 1 diabetes ?

A

no insulin produced=: -Increase in protolysis -increased HGO -increase lipolysis (if this is prolonged fatty acids are converted into ketone bodies =increase in ketone bodies)

33
Q

What is diabetic ketoacidosis?

A

If type 1 diabetes goes untreated for a prolonged period of time then too many ketone bodies are produced causing the blood to become acidic

-this is a serious acute complication which has a high mortality rate

34
Q

What are the symptoms of type 1 diabetes mellitus (T1DM)?

A

-weight loss(due to breakdown of protein) -high blood sugar -glycosuria (glucose in urine) with this you get osmotic symptoms(osmotic diaresis) -ketone bodies in the blood and urine

35
Q

osmotic diaresis symptoms?

A

polyuria- lots of urine noturia-passing urine at night polydipsia-thirst caused by the fact that your losing lots of urine and becoming dehydrated and have high blood glucose

36
Q

What are useful diagnostic tests for T1DM?

A

-test for antibodies:GAD, IA2 -c-peptide (low due to not producing insulin) -presence of ketones

37
Q

What happens if people with T1DM take too much insulin?

A

-switch of hepatic gluconeogenesis=reduced hepatic glucose output -glucose taken up by the muscle cells but if there is too much insulin then this keeps happening resulting in insulin induced HYPOGLYCAEMIA

38
Q

What is the counterregulatory response to hypoglycaemia?

A

increase in glucoagon, catecholamines, cortisol and GH -this causes the increase of hepatic glucose output with glycogenolysis and gluconeogenesis AND increased lipolysis

39
Q

What is impaired awareness of hypoglycaemia?

A

this is the reduced ability to recognise symptoms of hypoglycaemia This happens if body experiences many episodes of hypoglycaemia as your body starts to think this is normal so the counterregualtory sytem where hypoglycaemia is detected is still there but kicks in at a lower level of blood glucose than it should normally

40
Q

What are the symptoms of hypoglycaemia?

A

-Intitial symptoms are autonomic(when blood sugar levels are somewhere around 3): -Sweating -Pallor -Palpitations -Shaking Neuroglycopenci symptoms(whne blood glucose drops further and your brain is not getting enough glucose): -Slurred speech -Poor vision -Confusion -Seizures -Loss of consciousness

41
Q

What is the definition of a severe hypoglycaemic episode?

A

when a person needs a third party assistance to treat

42
Q

What is type 2 diabetes?

A

Insulin resistance in the liver, muscle and adipose tissue(metabolic sites)

-you have enough insulin to supress ketogenesis and proteolysis

43
Q

What pathways do insulin activate?

A

PI3K-Akt -metabolic actions

MAPK -growth and proliferation

44
Q

What happens in terms of insulin when you have insulin resistance?

A

Body doesnt respond properly to insulin, this causes more insulin to be produced

45
Q

Which insulin activated pathway is not insulin resistant?

What effect does this have?

A

MAPK

Therefore if you have type 2 diabetes and therefore have lots of extra insulin in the body you enhance the effects of this pathway=increased growth of smooth muscle in the artery=increased blood pressure

46
Q

How can you identify if someone has insulin resistance

A
  • They have high triglycerides
  • Low HDL
  • High blood pressure
  • High waist circumference due to weight gain
  • Insulin resistance leads to type 2 diabetes therefore fasting glucose is more than 6mmol/L -

\insulin resistance causes inflammation but cant measure this

47
Q

What are the symptoms of type 2 diabetes?

A
  • Hyperglycaemia
  • overweight
  • abnormal fats in their blood(dyslipidaemia)
  • less osmotic symptoms
  • insulin resistance
  • complications(eyes, kidneys, nerves in feet, stroke, heart,attacks, amputations)
  • later on get insulin deficiency caused by beta cell dysfunction so may need insulin tablets later on like those with T1DM
48
Q

What are some risk factors of type 2 diabetes?

A
  • age
  • high BMI
  • PCOS
  • Family
  • Inactivity
49
Q

What are dietary recommendations for those with diabetes?

A
  • calorie control
  • reduce calories from fat
  • reduce calorie intake from refined carbohydrates
  • Increase calorie intake from complex carbohydrates
  • increase soluble fibre
  • decrease sodium
50
Q

How can you manage T1DM?

A
  • take exogenous insulin(via injections-basal bolus regime, take insulin regularly throughout day)
  • self monitor of glucose 4-10 times a day
  • structures education -technology
  • flash glucose monitoring devise, insulin pumps
51
Q

How do you manage T2DM?

A
  • Diet
  • first line management
  • Oral medication
  • education
  • May need insulin eventually
52
Q

What can be done to help prevent long term diabetes related complications?

A

Monitor these things: -retinopathy -neuropathy -nephropathy -cardiovascular -optimal glucose control

Bio regulatory systems 2 (15 decks)

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