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Biochemistry > Glycolysis > Flashcards

Glycolysis Flashcards

1
Q

how is insulin release biphasic

A

1 preformed : within 15 min

2 gene level

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2
Q

name irreversible steps in glycolysis

A
  1. hexo/glucokinase
  2. phosphofructokinase 1
  3. pyruvate kinase
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3
Q

what fxn as glucose sensor in b cell of pancreas

A

glucokinase

glut 2

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4
Q

where is glucokinase found. comment on its Km

A

hepatocytes and b cell of pancreas

higher than hexokinase

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5
Q

effect of arsenate on glycolysis

A

forms 1arseno3phosphoglycerate which undergo hydolysis preventing atp formation

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6
Q

rate limiting and main control point in glycolysis

A

PK1

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7
Q

control of Pk1 by insulin and glucagon is indirect via PK2. True/false

A

true via 2,3 bisphosphoglycerate

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8
Q

mcc genetic cause of hemolytic anemia

A

G6PD def

2nd:pyruvate kinase def

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9
Q

diff G6PD and PK def

A

abscence of heinz bodies

inc 2,3-BPG

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10
Q

why aldose B def is severe

A

because it leads to accumulation of F1P in proximal renal tubules and liver
fructokinasecdef is benign

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11
Q

why no cataract formation in fructosemia

A

beacause fructose is a ketose

not met by aldose reductase in lens

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12
Q

def of gal 1 p tranferase is more sever2 tjan galactokinase

A

same reason

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13
Q

diagnosis of lactose intolerance based on

A

positive H2 breath test

bact breaks lactose to CH4 H2 and osmotically active organic acids

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14
Q

can milk product yoghurt be taken by LI person

A

yes, unpasteurised because it has lactobacillus to digest lactose

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15
Q

why a high fructose drink supplies quick energy then glucose

A

fructose 1 p products DHAP and G3P are downstream of the key reg of pathway PK1
it is not so with galactose it gets converted to glucose

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16
Q

can AcetyCoA be converted back to glucose

A

no

PD is an irreversible enzyme

17
Q

why thiamine given along with glucose in emergency

A

to prevent lactic acidosis when glycose/dextrose is given

18
Q 
thiamine
lipoic acid
CoA
FAD
NAD
A

PD
a ketoglutarate dehydrogenase
branched chain ketoacid dehydrogenase

19
Q

gycogen synthesis inhibited by

A

m:epinephrine
liver:epi+glucagon
via inhibition of glucagon phosphorylase
and stimaltion of synthase via insulin

20
Q

how is free glucose produced during glycogenolysis

A

as a result of debranching enzyme
1.breaks a1.4 bond and attach this oligoglucose to the exposed end of other chain to form new a 1.4 bond
2.hydrolyse the single a1.6 bond releasing the single residue as free glucose
since it is not a phosphorylase so no Pi is added to it

21
Q

von gierke:severe hypoglycemia
hers:mild
how?

A

in von gierke glucose cant come from either glycogenolysis or gluconeogenesis

22
Q

cardiomegaly in

A

pompe

23
Q

branching and debranching enz defect

A

anderson

cori

24
Q

features of von gierke

A
  1. glcogen deposits in liver:G6P inhibits lysis and promotes glycogen syn
  2. hyperuricemia:dec Pi and inc AMP
  3. hyperlipidemia and skin xanthoma
  4. fatty liver
25
Q 
what is the effect of blood glucose level if one of the following is administered.
glucagon
epi
fructose
galactose
A

none effects the level

26
Q

only ketogenic amino acids

A

leucine

lysine

27
Q

how is pyruvate converted to phosphoenolpyruvate during gluconeogenesis

A

pyruvate-goes in mitochondria-OAA-malate-shuttle-malate in cyto-OAA-phosphoenolpyruvic acid

28
Q

key control point of gluconeogenesis

A

fructose 1,6 bisphosphatase

29
Q

F 2,6 bisphoaphate by PK2 control glycolysis and gluconeogenesis
how

A

PK2 is + insulin

- gluvagon

30
Q

is glusose 6 phosphatase present only in liver

A

yes

31
Q

is glucose produced during gluconeogenesis used as a source of energy for liver

A

no
it is actually using f.a.
the energy of which is used in gluconeogenesis

32
Q

can fatty acids be used for gluconeogenesis

A

no.acetyl CoA cant be converted back to pyruvate

but odd chain fatty acids may yield propionly CoA

33
Q

biotin def

A

alopecia
scaly dermatitis
waxy pallor
acidosis

34
Q

why alcoholism is ass with hypoglycemia and fatty liver

A 
NAD-NADH no NAD  is free
high NADH leads to
1.lactate from pyruvate
2.malate from OAA in cyto
3.glycerol 3 P from DHAP
divert imp gluconeigenic substrates from enetering gluconeogenesis

When f.a come in liver

  1. high NADH slows oxidation
  2. combine with excess gl 6 P
35
Q

extreme ex and alcohol consumption

A

metabolic acidosis

36
Q

only thiamine containing enz in rbc

A

transketolase

37
Q

name X linked ds with heinz bodies

A

G6PD deficiency

Biochemistry (12 decks)

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