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Fuel Metabolism 2016 > carbs > Flashcards

carbs Flashcards

1
Q

lumen of small intestine (enzyme and digestion)

A

pancreatic amylase from cck, (neutral pH from secretin) oligo->disaccharide

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2
Q

brush border of small intestine

A

disacc picked up spit out as monosacc

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3
Q

brush border transporters 2

A

SGLT1 GLUT5. actively transports monos into cells using energy from na gradient

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4
Q

basolat glut transporter in small intestine

A

2, high capacity and low affinity (super sensitive) facillitated diffusion into blood,

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5
Q

GLUT2 properties

A

liver, pancreas, kidney, intestine, depends on glucose gradient, glucose flows in during fed state and out during fast

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6
Q

insulin dependent transporter and tissues

A

GLUT4, mobilized from vesivcles in fat skeletal and cardiac muscle

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7
Q

GLUT in blood and brain

A

1 AND 3, high affinity, ensures constant supply even at low glucose level

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8
Q

how does hyperglycemia result in complications during diabetes

A

aldol reductase similar to GLUT2, too much glucose causes sorbitol prod, causes accumulation and osmotic effect leading to tissue damage

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9
Q

frequency of glycogen branching

A

8-10 glucose units

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10
Q

energy required for glycogen synthesis per glucose

A

2 high energy phosphate bonds

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11
Q

what is activated glucose and why the need for pyroPO4

A

trap glucose in cell with a form that as sufficient energy to make a1-4 bond, PPi is used to couple rxn

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12
Q

insulin promotes __ by __

A

fuel storage by dephosphorylation

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13
Q

glucagon/epi promote __ by __

A

Fuel mobilization by phosphorylation

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14
Q

cAMP and glycogen

A

phosphorylates glycogen synthase through PKA, inactivating it

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15
Q

epi to beta activates

A

cAMP

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16
Q

epi to alpha activates

A

Ca2+

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17
Q

where is glucose entry insulin dependent

A

adipose and muscle

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18
Q

four compounds requiring galactose

A

glycoproteins glycolipids proteoglycans breast milk

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19
Q

difference in galactosemia between galactokinase and uridyl transferase deficiency

A

uridyl transferase def. results in buildup of galactose1po4, causing buildup of galactitol

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20
Q

how does HFI result in hypoglycemia even with sufficient glycogen stores?

A

Not enough phosphate to break glycogen down because it is backed up in fructose metabolism

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21
Q

toxic intermediate in etoh metab

A

acetaldehyde

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22
Q

how does disulfiram(antabuse) work

A

competitive inhibitor of ALDH, keeps acetaldehyde in the blood leading to increased hangover

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23
Q

how does fomepizole work

A

competitive inhibitor of ADH (like ethanol) for antifreeze poisoning

24
Q

what are the fates of pyruvate

A

acetyl co a, lactate, alanine, oxaloacetate

25
Q

what is the link between glycolysis and tca

A

pyruvate deghydrogenase complex

26
Q

coenzymes of PDH

A

CoA, NAD, FAD, Lipoic acid, Thiamine

27
Q

why would lactate or alanine accumulate

A

defect in converting to acetyl coa or oxaloacetate because pyruvate lactate and alanine are freely interconvertable

28
Q

what is beri beri

A

thiamine deficiency in diet

29
Q

how would treatment for genetic PDH deficiency differ from environmental

A

slowly give glucose to genetic, cannot handle large amounts

30
Q

what is arsenic poisoning

A

destroys the functionality of lipoic acid, making acetyl coa from PDH and pentose phosphate

31
Q

function of pentose phosphate

A

make nucleotides and nadp, recycling pentose phosphates back to glyceraldehyde-3-po4 in RBCs

32
Q

committed step in pentose po4 path

A

(G6P dehydrogenase) oxidation of G6P Gluconolactone, making NADPH

33
Q

thiamine deficiency rbcs diagnosed from

A

reduced transketolase activity

34
Q

four tissues where pentose phosphate is especially prominent

A

liver, adrenal, WBC, RBC

35
Q

why are antimalarials a no for people with G6P dehydrogenase deficiency

A

not enough NADPH to deal with increased ROS, causing anemia

36
Q

two ways NADPH protects RBCs

A

MetHB reductase, glutathione reductase (takes care of peroxide)

37
Q

how do phagocytes use NADPH

A

killing bacteria with free radical generation

38
Q

two molecules linking tca with respiratory chain

A

malate dehydrogenase, complex 2

39
Q

key regulated enzyme in tca

A

isocitrate dehydrogenase

40
Q

example of anapleoric rxn

A

pyruvate carboxylase: used to make oxaloacetate in gluconeogenesis, can be shunted for tca

41
Q

three sources of blood glucose

A

glycerol lactate amino acids - especially alanine (leucine and lysine cant)

42
Q

what is the cori cycle

A

cycles lactate from muscle to liver and glucose back to muscle

43
Q

four unique enzymes to gluconeogenesis

A

pyruvate carboxylase, PEPCK, f16bpase, g6pase`

44
Q

where is pyruvate caboxylase

A

mitochondria

45
Q

where are gluconeogenic enzymes localized

A

liver and kidney

46
Q

what does f26bp do

A

promote glycolysis inhibit gluconeogenesis

47
Q

what happens with b vitamin deficiency

A

decrease in gluconeogenesis and glycogenolysis

48
Q

mcardles disease and treatment

A

muscle isozyme of glycogen phosphorylase, limit strenuous activity and eat carbs before exercise

49
Q

deficient glycolytic enzyme leading to hemolytic anemia

A

pyruvate kinase (leads to the accumulation of 2,3-BPG, which

decreases the O2 affinity for Hemoglobin)

50
Q

GLUT 5 importance

A

fructose channel, Na independent, brush border of intestine,

51
Q

what does insulin do in the liver

A

induce synthesis of glucokinase

52
Q

what does insulin do in muscle

A

push GLUT4 receptors to cell surface

53
Q

what is McArdles diesease

A

disease of muscle glycogenolysis

54
Q

why is hfi more severe than essential fructosuria

A

hfi has phosphorylated fructose trapped in cells, also degrades atp and phosphate stores in liver, preventing glycogenolysis leading to hypoglycemia

55
Q

what is von gierkes disease

A

deficiency in glucose-6-phosphatase

56
Q

what is hers disease

A

glycogen phosphorylase deficiency in liver

Fuel Metabolism 2016 (6 decks)

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