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Re: Laurie/Barbara

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Laurie,

thanks for the explanation, it sure helped.

I do have another question as a result though.

I understand complex II is where the krebs cycle is brought in ,I assume this

is where the fatty acid takes place...if so would a defect in II cause a

increase in the fatty acids in blood and urine? Also would this also cause a

increase in the level of krebs cycle intermediates like fumurase and succinate

etc....?

I read in a article from a link from UMDF that a leighs like syndrome is

caused by a complex II defect and it is dominant or recessive and it causes a

increase in succinate and biopsy shows a partial defect in complex II with a

enzymatic deficiecny of 50-75% of complex II activity.

would a complex II level of 60% would be a partial defect????

Thanks again,

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You have got me here - I don't have a clue! This might be a good question

to ask at our next MDA chat with one of the specialists.

laurie

> From: Mrsmurffy@...

> Reply-To:

> Date: Mon, 31 May 2004 14:00:28 EDT

> To:

> Subject: Re: Laurie/Barbara

>

> Laurie,

> thanks for the explanation, it sure helped.

> I do have another question as a result though.

> I understand complex II is where the krebs cycle is brought in ,I assume this

> is where the fatty acid takes place...if so would a defect in II cause a

> increase in the fatty acids in blood and urine? Also would this also cause a

> increase in the level of krebs cycle intermediates like fumurase and succinate

> etc....?

> I read in a article from a link from UMDF that a leighs like syndrome is

> caused by a complex II defect and it is dominant or recessive and it causes a

> increase in succinate and biopsy shows a partial defect in complex II with a

> enzymatic deficiecny of 50-75% of complex II activity.

> would a complex II level of 60% would be a partial defect????

> Thanks again,

>

>

>

>

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I second Laurie's suggestion--ask the experts! I can just add that

many, if not most, people with inborn errors in fat metabolism have

essentially normal serum lipid profiles. The genetic FOD defects are

not diagnosed primarily by a derangement of lipids in blood because

this does not occur in many cases and because those findings can be

caused by many other conditions. Inborn errors in fat metabolism are

diagnosed by measursing the activity of the essential enzymes that

are catalysts for oxidizing fatty acids. Also--while fat metabolism

takes place primarily in beta oxidation, it is true that all these

metabolic cycles interact in complex ways. A defect in one cycle can

secondarily upset the balance in another cycle. Not sure that

helps....but it's all I can offer. :-)

B

>

>

> You have got me here - I don't have a clue! This might be a good

question

> to ask at our next MDA chat with one of the specialists.

>

> laurie

>

> > From: Mrsmurffy@a...

> > Reply-To:

> > Date: Mon, 31 May 2004 14:00:28 EDT

> > To:

> > Subject: Re: Laurie/Barbara

> >

> > Laurie,

> > thanks for the explanation, it sure helped.

> > I do have another question as a result though.

> > I understand complex II is where the krebs cycle is brought

in ,I assume this

> > is where the fatty acid takes place...if so would a defect in II

cause a

> > increase in the fatty acids in blood and urine? Also would this

also cause a

> > increase in the level of krebs cycle intermediates like fumurase

and succinate

> > etc....?

> > I read in a article from a link from UMDF that a leighs like

syndrome is

> > caused by a complex II defect and it is dominant or recessive

and it causes a

> > increase in succinate and biopsy shows a partial defect in

complex II with a

> > enzymatic deficiecny of 50-75% of complex II activity.

> > would a complex II level of 60% would be a partial defect????

> > Thanks again,

> >

> >

> >

> >

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