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HUNT241 > BIOC Lecture 11: Diabetes > Flashcards

BIOC Lecture 11: Diabetes Flashcards

1
Q

When is the age of type 1 onset?

A

Usually during childhood or puberty

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2
Q

What is the age of type 2 onset?

A

Frequently after age 35

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3
Q

What is the nutritional status at time of type 1 onset?

A

Frequently undernorished

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4
Q

What is the nutritional status at time of type 2 onset?

A

Obesity usually present

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5
Q

What is the prevalence of type 1 diabetes vs type 2?

A

Type 1 = 10%
Type 2 = 90%

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6
Q

What is the genetic predisposition of type 1 vs type 2?

A

Type 1 = moderate
Type 2 = very strong

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7
Q

What is the defect that causes Type 1?

A

Beta cells are destroyed, eliminating production of insulin

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8
Q

What is the defect that causes type 2?

A

Insulin resistance combined with inability of beta cells to produce appropriate quantities of insulin

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9
Q

What is the frequency of ketosis in type 1 vs type 2?

A

Type 1 = common
Type 2 = rare

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10
Q

What is plasma insulin in type 1 vs type 2?

A

Type 1 = low to absent
Type 2 = high early in disease, low in disease of long duration

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11
Q

What is the acute complications of type 1 vs type 2?

A

Type 1 = ketoacidosis
Type 2 = hyperosmolar state

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12
Q

What is the response to oral hypoglycemic drugs in type 1 vs type 2?

A

Type 1 = unresponsive
Type 2 = responsive

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13
Q

What is the treatment for type 1 diabetes?

A

Insulin is always necessary

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14
Q

What is the treatment for type 2 diabetes?

A

Diet, exercise, oral hypoglycemic drugs, reduction of risk factors (smoking, blood pressure)

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15
Q

What is glycosuria?

A

high glucose levels in urine

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16
Q

What is osmotic diuresis?

A

water will move into areas of high glucose concentration which leads to dehydration

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17
Q

What fasting glucose indicates diabetes?

A

> 7.0mmol/L (fasting)
11.1mmol/L (fed)

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18
Q

What is HbA1c?

A

Glycated hemoglobin - measure of longer-term glucose status

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19
Q

What HbA1c indicates diabetes?

A

> 50mmol/mol

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20
Q

What are other symptoms of diabetes?

A
  • Glycosuria, osmotic diuresis, dehydration
  • Ketoacidosis
  • Thirst, frequent urination, fatigue
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21
Q

What underlies developing type 2 diabetes?

A
  • Certain sensitive genotype
  • Metabolic stress
  • Inflammation
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22
Q

Why is being overweight such a strong risk factor for type 2 diabetes?

A

Being overweight causes inflammation and high metabolic/oxidative stress

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23
Q

How does obesity lead to T2D?

A
  1. Insulin resistance causes…
  2. Glucose intolerance causes…
  3. Metabolic syndrome causes…
  4. Type 2 diabetes
24
Q

What is metabolic syndrome?

A

a cluster of biochemical and physiological abnormalities associated with the development of cardiovascular disease and type 2 diabetes

25
Q

What does prediabetic insulin resistance look like in the blood after feeding?

A

A lot more insulin than normal people to get the same level of control - over time, the insulin resistance gets worse to a point where you lose the glucose control

26
Q

What do fasting glucose levels look like in diabetics?

A

Their fasting glucose levels are higher - levels never really get back down before the next meal whereas in normal people it spikes and then comes back down

27
Q

What is insulin resistance?

A

Reduced response to the same amount of insulin

28
Q

What happens to glucose, glycolysis and fatty acids from IR?

A

Glucose uptake, glycolysis and fatty acid uptake are decreased

29
Q

What happens to gluconeogenesis, lipolysis, fatty acid oxidation and ketogenesis from IR?

A

They are increased

30
Q

How is glucogenesis increased by IR?

A
  • The liver is putting out lots of glucose
  • Normally would be inhibited by insulin
  • There is no response to insulin, the normally low levels of glucagon during the fed state are much higher
  • Glucagon drives glucogenesis
31
Q

How is lipolysis increased by IR?

A
  • Insulin inhibits fat mobilization from adipocytes
  • IR means TAG’s and fatty acids are mobilized by HSL
  • HSL is usually inhibited by insulin
  • You get mobilization of fats and a lot of fatty acids coming back to the liver
32
Q

What does the influx of fatty acids back to the liver promote?

A

more fat being made and that ends up promoting VLDL production, this is part of the reason type 2 diabetics have high TAG levels

33
Q

What is the insulin receptor?

A

Tyrosine kinase receptor

34
Q

What needs to happen to the tyrosine kinase receptor for it to be activated?

A

there is tyrosine residues in its structure that need to be phosphorylated before it can be activated - once insulin binds it can promote auto phosphorylation

35
Q

What happens to tyrosine kinase once it is activated?

A

IRS proteins are recruited to the receptor once its been phosphorylated

36
Q

What do IRS proteins do?

A

recruit a whole lot of kinases which trigger downstream activation or inhibition of various proteins - Ultimately you end up in a response

37
Q

What is happening in the signalling pathway during IR?

A
  • Proteins are not being phosphorylated
  • Proteins are mis-phosphorylated
38
Q

What are the two theories of obesity causing oxidative stress?

A
  • increased flux of glucose and lipid metabolism
  • overstimulated NADH oxidases
    Both cause increased oxidative molecules
39
Q

What are examples of oxidative molecules?

A
  • Superoxide O2
  • Hydrogen peroxide H2O2
40
Q

How do increased oxidative molecules impact the insulin signalling pathway?

A
  • activate a lot of serine kinases
  • kinases can mis-phosphorylate proteins in pathway
  • can inactivate them and stop pathway from working
41
Q

How does an increased flux of glucose and lipid metabolism cause increased oxidative molecules?

A
  • obese people have increased flux of this metabolism
  • this ramps up ETC
  • high levels of superoxide and hydrogen peroxide are produced
42
Q

How do overstimulated NADH oxidases cause increase oxidative molecules?

A
  • NADH oxidases aim is to produce superoxide
  • in diabetes they are overstimulated
  • produce a lot of superoxide
43
Q

Are all tissues equally effected by insulin resistance?

A

No, i.e. TAG synthesis in liver is still very active during IR

44
Q

Diabetes can develop fatty…

A

Livers

45
Q

What does fatty livers lead to?

A

Cirrhosis

46
Q

What does endurance training do for glucose tolerance?

A

Enhances glucose tolerance

47
Q

What is metformin?

A

The most common drug used for type 2 diabetes

48
Q

What is metformin transported into the liver by?

A

Oct1

49
Q

What is the main goal of metformin?

A

Indirectly activates AMPK and downregulates mGPD which leads to a reduction in glucose production

50
Q

What is the role of AMP kinase?

A

Regulates a lot of metabolic pathways, alters activity of TF which reduce/alter genes in the gluconeogenic pathway

51
Q

What does AMP kinase ultimately reduce?

A

Gluconeogenesis by downregulating mGPD and regulating cellular energy homeostasis

52
Q

What is AMP kinase activated by?

A

high levels of AMP

53
Q

How does metformin increase AMP levels to activate AMP kinase?

A
  • Inhibits first complex in ETC
  • Slows ETC and reduces ATP
  • ATP to AMP ratio goes down because there is more AMP
54
Q

Once AMPK levels are increased, what enzyme is downregulated?

A

mGPD

55
Q

How does mGPD reduce gluconeogenesis?

A
  • downregulating mGPD causes increased NADH levels
  • increased NADH means more lactate is formed in the liver
  • therefore pyruvate that was being used for glucose production, is now being used to produce lactate

HUNT241 (22 decks)

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