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

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
``` what is the effect of blood glucose level if one of the following is administered. glucagon epi fructose galactose ```
none effects the level
26
only ketogenic amino acids
leucine | lysine
27
how is pyruvate converted to phosphoenolpyruvate during gluconeogenesis
pyruvate-goes in mitochondria-OAA-malate-shuttle-malate in cyto-OAA-phosphoenolpyruvic acid
28
key control point of gluconeogenesis
fructose 1,6 bisphosphatase
29
F 2,6 bisphoaphate by PK2 control glycolysis and gluconeogenesis how
PK2 is + insulin | - gluvagon
30
is glusose 6 phosphatase present only in liver
yes
31
is glucose produced during gluconeogenesis used as a source of energy for liver
no it is actually using f.a. the energy of which is used in gluconeogenesis
32
can fatty acids be used for gluconeogenesis
no.acetyl CoA cant be converted back to pyruvate | but odd chain fatty acids may yield propionly CoA
33
biotin def
alopecia scaly dermatitis waxy pallor acidosis
34
why alcoholism is ass with hypoglycemia and fatty liver
``` 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
extreme ex and alcohol consumption
metabolic acidosis
36
only thiamine containing enz in rbc
transketolase
37
name X linked ds with heinz bodies
G6PD deficiency