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MET2 > Normal And Deregulated Metabolism > Flashcards

Normal And Deregulated Metabolism Flashcards

1
Q

3 metabolic states of the body

A

Absorptive
Post absorptive/fasting
Prolonged fasting/starvation

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2
Q

What processes occur in the absorptive state

A

Glycogenesis
Lipogenesis
Glycolysis

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3
Q

What processes occur in the post absorptive state

A

Glycogenolysis
Lipolysis
Gluconeogenesis

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4
Q

Which tissue does not use glucose as fuel in the post absorptive state

A

Liver

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5
Q

Why does the brain need constant glucose supply

A

Glucose is sole fuel for brain
Doesn’t store glucose

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6
Q

How are free fatty acids used to generate acetyl CoA

A

Beta oxidation

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7
Q

How are amino acids used in Gluconeogenesis

A

Enter TCA cycle

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8
Q

Which process provides additional fuel during fasting

A

Ketogenesis

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9
Q

Which cells keep using glucose during fasting

A

Brain
Red blood cells

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10
Q

Where is glucose for brain and RBCs sourced during fasting

A

Hepatic and renal Gluconeogenesis

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11
Q

What is the main source of energy during prolonged fasting

A

Ketone bodies

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12
Q

When are ketone bodies synthesised

A

Prolonged fasting
Fasting
After prolonged exercise

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13
Q

Which 2 intracellular electrolyte stores are especially depleted in Starvation

A

phosphate and potassium

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14
Q

Re feeding syndrome

A

Hypophosphataemia, hypokalamia, and thiamine deficiency caused by already low serum levels due to starvation are further decreased due to transport of electrolytes into cells for synthesis of glycogen, triglycerides, and proteins

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15
Q

What triggers re feeding syndrome

A

Insulin release after starvation

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16
Q

What hormones inhibit and stimulate ketogenesis

A

Stim - glucagon
Inhibit - insulin

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17
Q

What does the liver use as substrates for gluconeogenesis in the post absorptive state

A

Amino acids
Lactate
Glycerol

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18
Q

What happens to excess CoA

A

Converted to ketone bodies by liver

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19
Q

What fuel sources can the brain use

A

Glucose
Ketone bodies

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20
Q

Diabetes mellitus

A

Insulin deficiency or resistance or both

21
Q

Type 1 diabetes

A

Disruption of insulin secreting cells causing very reduced or no insulin production

22
Q

Type 2 diabetes

A

Target cells have insulin resistance and insulin secreting cells cannot compensate

23
Q

Where are GLUT 4 receptors when blood glucose concentration is low

A

Inside cell

24
Q

How does insulin work when blood glucose is high

A

Binds to receptor -> autophosphosphorylation of receptor on tyrosine -> IRS can bind to receptor ->IRS phosphorylated on tyrosine -> binds to PI3K -> PI3K moves from cytoplasm -> GLUT 4 transporters insert on membrane

25
Q

What needs to happen to IRS for PI3K to bind

A

IRS must be phosphorylated on tyrosine

26
Q

What can cause insulin resistance

A

Decreased insulin receptor numbers
Decreased catalytic activity of receptor
Incr activity of tyrosine phosphatases
Decr GLUT 4 levels and function
Incr IRS receptor phosphorylation
Decr PI3K/Akt activity

27
Q

How can pro inflammatory cytokines, saturated FFAs, and amino acids cause insulin resistance

A

Phosphorylate IRS
incr IRS degradation

28
Q

What happens when insulin acts on resistant cells

A

Messaging cascade stopped before reaching GLUT 4

29
Q

What causes the signalling process caused by insulin binding to be halted in insulin resistant cells

A

IRS already phosphorylated so can’t be phosphorylated by receptor

30
Q

Hyperglucagonaemia

A

Excessive circulating glucagon levels

31
Q

What is islet compensation

A

Increase in beta cell size, number, and function in response to insulin resistance

32
Q

Why does islet compensation occur in response to insulin resistance

A

Glucose tolerance can be maintained by increased insulin secretion

33
Q

Do alpha or beta cells in islets of langerhans increase in diabetes

A

Beta

34
Q

What can cause hypoglycaemia in patients without diabetes

A

Critical illness
Counter regulatory hormone deficiencies
Insulin overproduction

35
Q

Symptoms of hypoglycaemia

A

Trembling
Palpitations
Sweating
anxiety
Hunger
Tingling
Confusion
Difficulty concentrating
Weakness
Vision changes
Dizziness
Tiredness
Seizures
Loss of consciousness
Coma

36
Q

Causes of hypoglycaemia in diabetics

A

Overuse of insulin
Skipping meals
Incr physical activity
Alcohol excess

37
Q

How does alcohol cause hypoglycaemia in diabetics

A

Inhibition of gluconeogenesis

38
Q

What can recurrent hypoglycaemia lead to

A

Suppression of normal physiological counter regulatory response
Impaired awareness of hypoglycaemia

39
Q

What impairs awareness of hypoglycaemia

A

Whole body adaptations to repeated insulin induced hypoglycaemia and impaired counter regulatory response

40
Q

How can the liver cause hyperglycaemia

A

Decr glycogen synthesis
Impaired lipogenesis
Incr Gluconeogenesis
Incr glycogenolysis

41
Q

How can muscles increase hyperglycaemia

A

Decr glucose uptake
Decr glycogen synthesis
Incr protein catabolism

42
Q

How can adipose increase hyperglycaemia

A

Decr glucose uptake
Decr lipogenesis
Incr lipolysis

43
Q

How can the polyol pathway cause cell damage

A

Oxidative stress
ROS production
AGE production

44
Q

How does the polypol pathway affect blood vessels

A

Oxidase damage to macromolecules, impaired NO signalling, and pro inflammatory signalling increases vasoconstriction and impairs vasodilation

45
Q

What pathways is excess glucose diverted to in hyperglycaemia

A

Polyol pathway
PKC pathway
AGE pathway

46
Q

What does the PKC pathway cause

A

Incr vascular permeability and occlusion
Incr ROS
Inflammation
Mitochondrial dysfucntion

47
Q

What does AGE stand for

A

Advanced glycation end products

48
Q

How does the AGE pathway damage cells

A

Production of AGE - cause
Protein Structure modifications
Gene expression
Pro inflam molecule secretion
Free radical production

MET2 (25 decks)

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