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carbohydrates > Galactose + fructose metabolism > Flashcards

Galactose + fructose metabolism Flashcards

1
Q

sucrose

A

glucose + fructose

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2
Q

2 pathways fructose can take

A

Mainly metabolised in liver
liver: fructokinase—aldolase B

extrahepatic tissues_ Hexokinse—glycolysis pathway

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3
Q

what property does hexokinase have

A

its not just specific to glucose works on fructose too

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4
Q

how are fructose 6 phosphate and fructose 1 phosphat produced

A

liver _ fructose 1 p produced

extrahepatic - fructose 6 phosphat

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5
Q

job of aldolase B

A

in the liver

converts fructose 1 p into GAP and DHAPN

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6
Q

clinical cases for fructose

A

due to a deficiency of fructokinase. you get an accumulation of fructose in blood (4x5) release in urine -MELITURIA (sugar in urine)

howver is metabolised normally in the muscles where there is no defect .

deficiency of aldolase B in liver :
a build up of fructose 1 p which has an inhibitory effect on fructokinase leading to fructosuria

vomit - after ingesting sucrose
hyperphosphatemia- phosphate pook gets less so cant make atp- liver damage
inhibition of gluconeogenesis and glycogenolysis - which leads to hypoglcyemia

treatment- avoid sucrose

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7
Q

how is fructose absorbed

A

by glut 5 faciliated diffusion

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8
Q

how is galactose absorbed

A

S GLUT - secondary active transport (the same as glucose)

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9
Q

which 2 monosacchardes are epimers

A

glucose and galactose

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10
Q

how is lactose broken down

A

galactosidase

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11
Q

metabolism of galactose

A

like fructose its mainly in the liver but can be in extrahepatic tissues too

liver :
galactokinans forms galactose 1 phopshate

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12
Q

how does glucose 1 phosphate become glucose 6 p

A

phosphoglucomutase

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13
Q

clinical cases with galactose

A

galactokinase deficiency
causes elevation of galactose in blood - galactosemia and urine galactosuria.

galctosemia can be caused by a defect of 3 enzymes

  • galactokinase
  • GALT
  • UDP galactose 4 epimerase

when too much galactose it gets reduced in the eye by enzyme aldose reductase to form galacttitiol - cataracts

classical_
deficiency of GALT
build up of galactose 1 p
high level inhibits galactokinase and glucose metabolism

symptoms
increase eye presure 
brain damage 
short rbc survival + hemolysis
hypoglycemia
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14
Q

non classical galactosemia and classical

A

classical - deficincy of GALT - galactose 1 phosphate uridyl transferase

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15
Q

leloir pathway

A

galactose

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16
Q

STRUCTURE OF glycolgen

A

linear part _ a1/4 glycosidic bond
branched - 1,6 glycoside bond
majority is a- 1/4
glycogen has a protein called glycogenin

17
Q

glycogenolysis

A

3 enzymes involved
-glycogen phosphorylase- only breaks a 1/4 glycosidic bonds and stops 4 residues away from a 1/6 glycosidic bond
-glycogen debranching enzyme- remodel is a bifunctional enzyme that contains 2 different catalytic sites catalysing 2 different reactions
consists of glucan transferase-
amylo a 1/6 glucosidase- breaks 1-6 bond
-phosphoglucomutase

  1. release glucose 1 p
  2. restructure the glycogen molecule (so you can release more glucose 1 p)
  3. convert 1 to 6
18
Q

glucose 6 phosphatase

A

found only in gluconeogenesis organs so liver, kidney sI

19
Q

what is the fat of glucose 6 phosphate

A
  1. glycoloysis- muscles
  2. PPP
  3. gluconeogenenesis in liver
20
Q

when we break down glycogen what are the proportions of glucose 1 p and actual glucose

A

only 10 % is actual glucose

90% is glucose 1 phosphate

21
Q

glycogenosis

A

glucose —–glucose 6 p—–glucose 1 p—-glycogen

  1. hexokinase
  2. phopshoglucomutase
  3. glycogenn synthase
22
Q

glycogen synthase

A

uses UDP glucose as a substrate releasing UDP in the process

can’t begin from scratch needs a primer of more than 4 glucose monomers long

also just like glycogen phosphorolase it can only add 1-4 bonds

23
Q

how do we form udp glucose to form glycogen

A

glucose 1 p + UTP——udp glucose pyrophosphorylase—-UDP glucose

24
Q

enzymes involved in glycogen synthesis

A
  1. glycogen synthase

2. glycogen branching enzyme

25
Q

glycogen branching enzyme

A

cleaves off 7 or more residues

another chain cannot be added to close to a prexisting chain , has to be at least 4 residues away

26
Q

glycogen phosphorylase co enzyme

A

PLP

27
Q

glycogen phosphorolase regulation

A

has 2 isozymes
liver -
muscles

28
Q

glycogen synthase regulation

A
  1. OP - inactive
    OH- active

activated by insulin

29
Q

clinical cases regarding glycogen

A

glycogen storage disease are enzyme disorders affecting with glycogen synthesis or breakdown, typically within liver cells or muscle cells

liver- hypoglycemic
muscle- weak muscles especially when exercising

type 1 - von Gierke
type 2 - pompe - unable to degrade glycogen in lysoosmes due to glucosidase enzyme deficiency
type 3 - absence of debranch- Forbes
type 4 - absence of branch- Andersons
type 5 - abscence of phosphorolase - Mc ardles

30
Q

clinical cases regarding glycogen

A

glycogen storage disease are enzyme disorders affecting with glycogen synthesis or breakdown, typically within liver cells or muscle cells

liver- hypoglycemic
muscle- weak muscles especially when exercising

type 1 - von Gierke
type 2 - pompe - unable to degrade glycogen in lysoosmes due to glucosidase enzyme deficiency
type 3 - absence of debranch- Forbes
type 4 - absence of branch- Andersons
type 5 - absence of phosphorolase - Mc ardles

31
Q

where does gluconeogenesis take place

A

liver

kidney

32
Q

aa producing glucose

A

either get degraded to alanine or oxaloacetate which lead to glucose

33
Q

what cofactor does hexokinase use

A

Mg

34
Q

committed step in glycolysis

A

phosphofructokinase

35
Q

job of aldolase in glycolysis

A

break down fructose 1, 6 biphosphate is into DHAP and glycerladehyde 3 p

36
Q

what happens to the DHAP produced in glycolysis

A

needs to be converted to GAP via enzyme TP isomerase

37
Q

how many NADH produced from glycolysis

A

2

carbohydrates (1 decks)

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