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HUNT 241 > Lecture 10 - Dysregulation of Glucose and Fat Metabolism > Flashcards

Lecture 10 - Dysregulation of Glucose and Fat Metabolism Flashcards

1
Q

what is the genetic predisposition of type 1 diabetes compared with type 2

A

type 1 = moderate

type 2 = very strong

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2
Q

what is the frequency of ketosis in type 1 and type 2 diabetes

A

type 1 = common

type 2 = rare

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3
Q

what is the problem in type 1 diabetes

A

B cells are destroyed, eliminating production of insulin

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4
Q

what is the problem in type 2 diabetes

A

insulin resistance combined with inability of B cells to produce appropriate quantities of insulin

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5
Q

what is the fasting + random glucose level that is a symptom of diabetes

A

fasting glucose > 7mmol/L or random >11.1 mmol/L

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6
Q

what level of HbA1c be a symptom of diabetes and why

A

HbA1c > 50 mmol/mol

  • higher levels than this would suggest that you have had elevated glucose levels for sometime
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7
Q

what are some symptoms of diabetes

A
  • thirst
  • frequent urination
  • fatigue
  • hyperventilation
  • blurred vision
  • coma
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8
Q

what are glycosuria, osmotic diuresis and dehydration common symptoms of

A

diabetes

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9
Q

what are the three stages that lead to the development of diabetes from obesity

A
  • obesity
  • insulin resistance
  • glucose intolerance
  • metabolic syndrome
  • type 2 diabetes
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10
Q

what can not be distinguished between a normal and obese pre diabetic

A

can not distinguish between the obese and normal patient from glucose levels in the blood

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11
Q

what do insulin resistant obese people require more of

A

require more insulin to get the same glucose control as a normal person

= this is what you can the difference btwn normal and obese on graph

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12
Q

over time what happens to a insulin resistant diabetic over time in the control of blood glucose

A

over time, lose the control of blood glucose as their levels are constantly high and never properly go back down before the next meal

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13
Q

what does insulin resistance mean

A

reduced response to the same amount of insulin

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14
Q

what does hyperinsulinaemia diminish

A

the ability of b cells to respond to further increase in blood glucose

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15
Q

during insulin resistance, what happens to the processes that are normally stimulated by insulin

A

they arent stimulated

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16
Q

during insulin resistance, what happens to the processes that are normally inhibited by insulin

A

they aren’t inhibited

17
Q

what are things that are normally stimulated which aren’t during insulin resistance (what happens to them)

A
  • glucose uptake
  • glycolysis
  • fatty acid uptake

are decreased

18
Q

what are things that are normally inhibited which aren’t during insulin resistance (what happens to them)

A
  • gluconeogenesis
  • lipolysis
  • fatty acid oxidation
  • ketogenesis

are increased

19
Q

what happens to gluconeogenesis and fat mobilisation in type 2 diabetes

A

processes are increased as they are no longer inhibited by insulin

20
Q

what happens to the phosphorylation of proteins in the signalling pathway during insulin resistance

A

some proteins that would usually be phosphorylated are either not or incorrectly phosphorylated

21
Q

what are the two theories about how insulin resistance develops and what is there evidence that they both do

A
  • oxidative stress
  • inflammation

evidence that they both alter the insulin signalling pathway

22
Q

how does oxidative stress lead to insulin resistance

A

overweight people often have a high flux of glucose and lipid into the mitochondria

high activity of the electron transport chain can cause oxidative stress

this can cause miss phosphorylation of parts of the insulin signalling pathway

23
Q

how does inflammation lead to insulin resistance

A

pro-inflammatory cytokines can activate serine/threonine kinases, which can interrupt the normal pathway of insulin signalling

24
Q

are all tissues and pathways affected equally by insulin resistance

A

no

25
Q

diabetics can develop fatty livers which can lead to what and what does this tell us about triglyceride synthesis

A

can lead to cirrhosis

this tells us triglyceride synthesis is still going on in the liver

26
Q

in insulin resistant states what happens to the mobilisation of fats and therefore what is there more of in the liver and more of what will be produced

A

greater mobilisation of fats, therefore more TAG in the liver due to increased mobilisation of fats

more VLDL is produced to try export the extra fat from the liver

27
Q

in insulin resistant states LDL is not being hydrolysed so more what is released from the liver

A

more VLDL is released from the liver

28
Q

in insulin resistant states lipoprotein lipase is not stimulated, what does this mean

A

there is more chylomicron and remnant fatty acid into the liver

29
Q

insulin stimulates lipogensis, what happens in insulin resistant states and what does it lead to

A

this pathway is not effected, this leads to fatty liver as other pathways are inhibited but this isnt

30
Q

what happens in adipose tissue in insulin resistant states

A

increased delivery of fatty acids to liver via increased lipolysis due to increased HSL activity in adipose

31
Q

what happens in adipose and muscle tissue in insulin resistant states

A

VLDL remnant particles have increased triglyceride content due to reduction in LpL activity = increased blood TAGs

32
Q

treatment of type 2 diabetes

A

lifestyle changes

drugs = e.g metformin

33
Q

how does endurance training enhance your glucose tolerance

A

exercise will increase your insulin sensitivity

34
Q

what does the drug Metformin inhibit and what does this slow

A

mitochondrial electron complex 1, slows ETC and reduces ATP production

35
Q

as Metformin reduces ATP production what will increase

A

AMP will increase

36
Q

what will increased AMP levels increase and what will that activate

A

increased AMP will increase AMPK, which will activate transcription factors that will impact proteins in the gluconeogenesis pathway

37
Q

what will increased AMPK down regulate

A

mGPD enzyme (glycogen phosphate dehydrogenase)

38
Q

what will decreased mGPD do

A

increase NADH, meaning more lactate will be formed

HUNT 241 (19 decks)

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