non-glucose sugars and pentose shunt Flashcards by Rebecca Ruthberg

how do we trap galactose inside cell

phosphorylate

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how do we trap fructose inside cell

phosphorylate

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how do we trap glucose inside cell

phosphorylate

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hepatocytes have what transporter

GLUT2

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fructose comes from

sucrose

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aldolaes B is found in

liver

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is fructose 1-P an intermediate in glycolysis

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in liver, how is aldolase b used

backwards. so when pts fasting the liver will have problems

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if there is deficiency of aldolase b what disease

hereditary fructose intolerance

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pts who have hereditary fructose intolerance, what symptoms

Hypoglycaemia, and lactic acidosemia, vomiting, haemorrhage, hepatomegaly, renal dysfunction, hyperuricaemia, lacticacidaemia, cataracts

esp. when pt is fasting

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how is hereditary fructose intolerance treated

dietary restriction of fructose, sucrose and sorbitol

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fructose metabolism takes place primarily where

in liver

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in fructose metabolism, what is rate limiting step

aldolase b

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soribitol pathway, what is function

synthesis of fructose from glucose via sorbitol

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in sorbitol pathway glucose is reduced to sorbitol by

aldose reductase

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in sorbitol pathway sorbitol is oxidised to fructose by

sorbitol dehydrogenase

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where is sorbitol pathway esp. used

in seminal vesicles (sperm need fructose!)

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sorbitol

cannot leave cell, there is no transporter for it

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can sorbitol ever leave the cell

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if there is a lot of glucose, the cell will accumulate a lot of

sorbitol

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describe what happens in eye regarding sorbitol

there is a lot of glucose b/c it needs a lot of it for energy. aldose reductase is active but soribtol dehydrogenase has lower activity - it can accumulate soribotl. if there is too much glucose then too much soribtol and cause damage to eye.

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what is function of aldose reductase

glucose →sorbitol

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what is function of sorbitol dehydrogenase

sorbitol → fructose

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go through mechanism of fructose-induced cataracts

pg 10

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obesity endemic takes off b/c of

high fructose corn syrup (among other things)

fructose goes to cells and is trapped in cells as

fructose 1 phosphate

describe how high fructose corn syrup causes obesity

fructose 1 phosphate, fructose metabolism, so you bipass the PFK step which is major regulatory step in glycolysis, since we bipass the regulatory step then we don't have regulation of glycolysis. we don't regulate pyruvate, and pyruvate can be turned into fat.

glucose and galactose are

epimers

galactose 1-P is utilized by what enzyme

galactose 1-phosphate uridyltransferase

draw out galactose 1-P and UDP glucose reaction

pg 12 (just do the important step)

galactose kinase deficiency

if galactose doesn't stay in cell, blood gets flooded with galactose and have galactose hyperanemia. this could cause lenses to get clouded or cataracts.

galactose uptake is independent of what

insulin

in intestine lactase hydrolysise lactose to yield

glucose & galactose by breaking ß-1,4 linkage

show galactose to galactose 1-P step

pg 12

Classical galactosaemia (GALT deficiency) can lead to

cataracts

how can lactose intolerant mother breastfeed

mom produces galactosyltransferase, when she has baby then protein B (lactalbumin) will catalyse condensation of glucose and galactose to make lactose

what pathway is essential ina ll cells to provide NADPH for reductive detoxification

pentose phosphate pathway

what is pentose phosphate pathway used for

Pathway essential in all cells to provide NADPH for reductive detoxification and in most cells to provide ribose 5-P for nucleotide synthesis

bottom line of pentose phosphate pathway

NADPH is used

why is NADPH needed

synthesis (cholesterol, fatty acids, hormones) | anabolism

ribose 5-P is precuroser of

nucleic acids

what is needed in rapidly dividing cells

pentose phosphate pathway

give general summary of pentose pathway

oxidative reaction makaes NADPH | nonoxidative pathway makes ribose 5P

the oxidative phase of pentose pathway produces

NADPH and pentose

transketolase is enzyme that does what

Transketolase transfers a 2-C fragment from xylulose 5-P releasing glyceraldehyde 3-P pg 23

transketolase needs what

thiamine -PP (a vitamin)

thiamine PP is a

vitamin

NADPH in RBC is used to do what

RBC are exposed to oxidative stress. | NADPH is needed to make sure H2O2 won't harm the cell

what produces NADPH

pentose phosphate pathway

draw out mechanism for how NADPH allows RBC to avoid oxidative stress

pg 26

what are the precipitating factors of G6PD deficiency

oxidant drugs favism infection

UDP-sugars are what form of sugar

activated

where is UDP glucose formed

glycogen synthesis pathway

where would mutation be in classical galactosemia?

draw out, see pg 14

where would mutation be in nonclassical galactosemia

draw out, see pg 14

if galactitol is converted by aldose reductase what can happen in infants

cataracts

what happens if ribose 5p has been produced but isn't needed for nucleotide synthesis

it's converted to glycolytic intermediates

if cell needs NADPH, what does it do to fructose 6-P

converts it to glucose 6-P

the conversion of glycolytic intermediates to ribose 5-P is what kind of reaction

reversible

if cell has enough NADPH but needs ribose 5-P what does it do

inhibits oxidative path. ribose 5-P synthesized from glycolytic intermediates

what is NADPH's role in regulating pentose phosphate pathway

When NADPH is forming faster than it is being used for biosynthesis and glutathione reduction, [NADPH] rises and inhibits the first enzyme in the pentose phosphate pathway. As a result, more glucose 6-phosphate is available for glycolysis. (pg 22)

do RBCs generate NADPH?

why is NADPH used instead of NADH in reductive rxns requiring input of electrons

because NADPH/NADP+ ratio >> NADH/NAD+ | NADH rapidly oxidised back to NAD+ by ETC so [NADH] is low

look at G6PD deficiency slide and understand generally

pg 27

what is a key component of antioxidant defences

glutathione

what is the major antioxidant in the fluid lining the bronchial epithelium

glutathione

draw glutathione reductase reaction

pg 28

lactose is made out of

glucose & galactose

sucrose is made out of

glucose & fructose

what happens to disaccharides to be of use in glycolysis

they are hydrolyzed

what can convert to G6P

glucose, fructose, galactose, mannose

name five different fates of G6P in the liver

Dephosphorylate to yield free glucose to send to other tissues Make into liver glycogen Enter glycolysis, make acetyl CoA and then ATP for hepatocytes themselves Enter glycolysis, make acetyl CoA to be made into fatty acids and then TAGs Enter pentose phosphate pathway to yield NADPH and ribose-5-phosphate

what transporter in hepatocytes allows the passive diffusion of glucose

GLUT2 transporter

hepatocytes don't have hexokinase, they have

glucokinase

what is difference b/w glucokinase and hexokinase

glucokinase has higher km (g6p isn't made when glucose is low) glucokinase isn't inhibited by g6p, so it will just keep being made to g6p

draw the two rate limiting steps in fructose metabolism

pg 6

what does fructose metabolism generate that is an intermediate of glycolysis

glyceraldehyde 3-P & DHAP

how does fructose enter epithelial cells

GLUT5

GLUT5 is

insulin independent

what happens to fructose when it enters epithelial cells

it is rapidly phosphorylated to fructose 1 phosphate by fructokinase

if there is a deficiency in fructokinase, what disease

Essential Fructosuria

if there is fructose malabsorption, it will affect what

affects uptake of tryptophan resulting in deficiency of melatonin & serotonin.