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FBS 1 metabolism > fed and fasting > Flashcards

fed and fasting Flashcards

1
Q

main hormones of metabolism

A
  • insulin: hypoglycaemic hormone
  • glucagon: hyperglycaemic
  • adrenaline: in adrenal medulla
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2
Q

other insulin counter regulatory hormones

A

adrenaline - adrenal medulla
cortisol - adrenal cortex
growth hormone. - anterior pituitary

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3
Q

islets of langerhans

3 types of cells

A 
2% pancreatic mass
adult: 1million islets
B cells (60-70%) secrete insulin
a cells (30-40%) secrete glucagon
delta cells secrete somatostatin
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4
Q

insulin secretion stimulated by

A
  • increase blood glucose
  • increase amino acid conc
  • gut hormones: secretin and other GI hormones
  • glucagon: fine tune glucose homeostasis
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5
Q

insulin inhibited by..

A

adrenaline

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6
Q

describe steps to insulin secretion

A
  1. glucose
  2. glycolysis - production of ATP (metabolise a.acid)
  3. block K channels
  4. Ca channels open
  5. Ca increases in cell
  6. vesicle containing insulin secreted
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7
Q

what is secretion of glucagon stimulated bu

A
  1. low blood glucose
  2. high conc of amino acid in blood (prevent hypoglycaemia after protein meal)
  3. adrenaline: block insulin secretion.
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8
Q

metabolic effects of insulin

A
  • promote fuel storage after meal
  • promote growth
  • stimulate glycogen synthesis and storage
  • stim fatty acid synth and storage from CHO when intake exceeds glycogen storing capacity
  • stim amino acid uptake and protein synthesis (liver and muscle cells)
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9
Q

role of insulin in terms of receptors on diff tissues

A
  • -promote GLUT4 transporters in muscle and adipose tissue
  • brain, liver, erythrocyte and pancreas have GLUT - not insulin dependent
  • high insulin conc = down-regulation of its receptors
  • effects vary in time: Glc transporters and activation is rapid, synthesis of enzymes is slow
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10
Q

what does glucagon do during fasting

A
  • mobilise fuel and maintain blood glc during fasting
  • activate glycogenolysis and gluconeogenesis in liver
  • activate a.acid uptake by liver for gluconeogenesis
  • FA release from adipose tissue
  • FA oxidation and ketone boy formation in liver
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11
Q

what does adrenaline do during stress

A

mobilise fuel during stress:

  • stim glycogenolysis (muscle and liver)
  • stim FA release from adipose tissue
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12
Q

what does cortisol do

A

provide long term needs:

  • stim aa mobilisation from muscle
  • stim gluconeogenesis
  • FA release fro adipose tissue
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13
Q

fed (absorptive) state:
when is it
main things that happen during this time in terms of glucose, aacid, TAG

A

2-4 hrs after meal

  • increase blood glucose,, amino acids and TAG as chylomicrons
  • synth/store glycogen, TAG and protein
  • liver receives nutrients before other tissues - hepatic portal vein
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14
Q

when does the liver do gluconeogen and explain why

A
  • liver does gluconeogenesis always except in fed state (high insulin/glucagon ratio)
  • glycogen synthase active, phosphorylase inhibited
  • high Km for glucose = no competition with brain when glc low
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15
Q

how is glycolysis activated in the liver

A

fed state: activate glucokinase.

also activated through PFK and pyruvate kinase

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16
Q

describe liver fat metabolism

A
  • FA and TAG synthesis activated
  • acetyl CoA carboxylase activated
  • malonyl CoA inhibits carnitine transferase
  • new FA becomes esterified to TAG - does not enter mitochondrion for oxidation
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17
Q

brain and erythrocyte

A
  • rely on glc: FA can’t cross blood-brain barrier and erythrocyte has no mitochondria
  • glc transport is independent of insulin (GLUT1)
  • use of glc at high and low conc
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18
Q

muscle

A
  • GLUT4 transporters increase in number
  • activate glycogen synthesise and inhibit phosphorylase in liver
  • activate amino acid uptake and increase protein synthesis
19
Q

adipose tissue

A
  • lipoprotein lipase activated by insulin. Allows entry of FA for esterification and storage of TAG
  • GLUT4
  • glc needed to produce glycerol phosphate and esterification of TAG
  • hormone sensitive lipase: inhibited so TAG isn’t degraded
20
Q

fasting state (post-absorptive)

A
  • blood glc peak an hour after eating
  • normal blood 2 hrs after meal
  • blood glc removed for oxidation or storage
  • glucagon conc rises, insulin drops
21
Q

fasting: liver and adipose

A
  • liver maintains blood glc conc at 4mM
  • adipose provides most energy as TAGs
  • hormone sensitive lipase activated by glucagon and adrenaline
  • FA transported to liver boun to albumin
22
Q

glucose production by liver (fasting)

A
  • glycogen
  • gluconeogenesis follows from lactate (erythrocytes and muscle, glycerol (adipose), amino acids (muscle)
  • after 24hrs fasting, all blood glc comes from gluconeogenesis
23
Q

why can’t FA be used to make glucose (fasting) in liver

A
  • FA is nto a gluconeogenic precursor
  • pyruvate dehydrgenase reaction (pyruvate->acetyl CoA) is irreversible
  • PDH activated by insulin, inhibited by glucagon
  • ensure gluconeogenic substrates channeled into glc production, not A.CoA. (we get enough CoA from FA)
24
Q

how is conversion of pyruvate to acetyl CoA inhibited

A

insulin??

acetyl CoA inhibits pyruvate hydrogenase.

25
Q

what are 2 ketone bodies released into the bloodstream

A

acetoacetate and B-hydroxybutyrate

26
Q

why are ketone bodies used

A

too many acetyl CoA made by oxidation of FA to enter the TCA cycle.
Most tissues oxidise a mix of FA and KB
erythrocytes use glucose, brain uses glc and KB

27
Q

how much protein can be used in prolonged starvation before fatal consequences

A

a third of body protein

28
Q

explain the difference in urea excretion in fed and fasting state

A

large amount of urea produced 12hrs after food. decreases 3 days and 5-6weeks after.
Lots of muscle breakdown at the start.
decreases as the brain is using ketone bodies, so less muscle breakdown

29
Q

what happens as starvation continues?

A
  • muscles use FA rather than KB
  • [FA] plateau, KB rise
  • brain can use more KB, less glucose
  • need for gluconeogenesis is reduced, muscle protein breakdown decreases
  • less urea production
30
Q

what do ketone bodies do?

A

-act on pancreatic B cells - stimulate insulin release
-limits muscle proteolysis
-limits adipose tissue lipolysis
preserves muscle tissue.

31
Q

what events lead up to death?

A

fuel exhaustion, loss of function due to loss of protein, impairment of immune system

32
Q

what is an important determinant of survival?

A

amount of adipose tissue

33
Q

how long can one starve for before death?

A

40days (perhaps longer if young and fit)

death from starvation often due to infection

34
Q

other names for type 1 and 2 diabetes

A

1: insulin dependent diabetes mellitus IDDM
2: non-insulin dependent diabetes mellitus
10-20% diabetics are IDD

35
Q

diabetes

A

2-3% pop affected
90% endocrine disorders
cause blindness, amputations, premature deaths
-5-10% total health care budget

36
Q

diabetes type 1: cause, symptoms and treatment

A
  • autoimmune destruction of B cells
  • early onset
  • polyuria, polydipsia, polyphagia (excessive eating), fatigue, weight loss, muscle wasting, weakness
  • hyperglycaemia, ketoacidosis
  • insulin treatment
37
Q

diabetes type 2: cause, symptoms and treatment

A
  • later onset
  • insulin resistance
  • diet and lifestyle
  • hyperglycaemia but no ketoacidosis
  • diet and oral hypoglycaemic agents
38
Q

what are the metabolic patterns during starvation in a diabetic

A

similar response to starvation but more exaggerated:

  • low insulin (type 1-absent)
  • unopposed glucagon acts
  • KB produced in starvation = insulin release
  • limit muscle protein breakdown, release of FA from adipocytes and uncontrolled production of KB
  • this important mechanism does NOT operate in diabetes
39
Q

Chronic complications of diabetes mellitus

A

Microangiopathy: changes in walls of small blood vessels seen as thickening of basement membrane
• Retinopathy: blindness is 25 x more common in the diabetic patient
• Nephropathy: renal failure 17 x more common
• Neuropathy: postural hypotension, impotence, foot ulcers

40
Q

treatment of diabetes 1

A

1: exogenous insulin by injection. Important to balance dosage with amount of food to avoid hypoglycaemic incidents, the most common complication of insulin therapy

41
Q

treatment of diabetes 2

A

2:weight reduction, dietary modification, oral hypoglycaemic agents
• biguanides increase the number of glut4
• sulphonylureas act on the β cell to improve insulin secretion

42
Q

describe metabolic syndrome

A 
WHO:
Metabolic syndrome
• High fasting glc/insulin resistance/diabetes type 2/impaired GT
• Plus2of:
• Hypertension
• Dyslipidaemia (high TAG/low HDL
• Central obesity
• microalbuminuria
43
Q

metabolism in diabetes

A
  • excessive protein breakdown
  • excessive gluconeogenesis
  • fat breakdown, leading to KB production
  • unopposed

FBS 1 metabolism (10 decks)

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