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Vitamin D discovery outpaces FDA decision making
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  1  2  3  4  5  6   
 

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Russ
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 Posted: Tue Aug 19th, 2008 09:23

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Yeah, I've heard that explanation before, though more in terms of just that they gnawed on bones rather than completely ate them.  So yeah, if that's true, I guess they would have gotten a lot more calcium than I was thinking.



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 Posted: Tue Aug 19th, 2008 10:17

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Calcium is found in leafy vegetables and seeds.
 

JudyBeauty
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 Posted: Tue Aug 19th, 2008 13:29

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I bet primitive man ate lots of insects which contain calcium.  There are many cultures today that still eat insects and seem to enjoy them.



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 Posted: Mon Sep 8th, 2008 17:54

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Take a look at this from the Parade Magazine from yesterday.

Vitamin D & Heart Disease

A report published in Archives of Internal Medicine suggests that a vitamin D deficiency can worsen heart disease.  Researchers looked at levels of the vitamin among more than 3000 Austrians who were in the hospital for heart procedures.  Seven years later, those who'd that the lowest vitamin D levels were most likely to have died in the interim.  Another study, in the Journal of Cardiovascular Pharmacology, reports that vitamin D seems to help ward off heart failure-at least in rats.

"The sunshine vitamin" - technically is not a vitamin but a steroid hormone-gets activated when skin is exposed to sunlight.  As little as 10 minutes of exposure daily may be enough to prevent low levels, also linked to broken bones, high blood pressure, cancer, and immune-system problems.

My purpose in sharing this is that I am surprised to finally see somewhere written that vitamin D is a steroid hormone besides from Dr. Marshalls papers.  Looks like they may be trying to catch up.  ;)

All the more reason for those who have chronic diseases to stay out of the sun so that the immune system is not suppressed.

Saj

 

Saj



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inge
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 Posted: Wed Oct 8th, 2008 07:00

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In Marshall's Bioessays paper vitamin Ds are metioned as putative PXR-antagonists. While this may not be well documented, is there any doubt at all that 25-vit D and 1,25-vit D will affect CYP27A1, irrespective of the mechanism?  To me it seems that this is well documented, but this is perhaps solely based on animal studies?

One more thing: Why is there a question mark between the two PXR bubbles in Figure 1?

Inge  



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 Posted: Wed Oct 8th, 2008 07:16

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There is now no doubt that the Vitamins D are PXR antagonists. I had correspondence with a wet-biology group who had tested Vitamin D as a PXR agonist, and it failed, so now we know the pathway - antagonism, which is the only one which makes sense, in any case.

The green question mark indicates that we really don't know what ligand activates PXR to transcribe CYP27A1, CYP24 or CYP3A4.
 
 

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 Posted: Fri Aug 14th, 2009 10:28

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Trevor,

I was wondeering if you are keeping the model from the BioEssays paper up to date? Changing colors when pathways are confirmed and perhaps adding pathways ?

I just ran into this paper, that seems to add to the model downregulation of hydroxylation via cyp2R1 and perhaps more, but you be the judge, it is hard to judge from an abstract, but seems promising:

Regulation of human vitamin D(3) 25-hydroxylases in dermal fibroblasts and prostate cancer LNCaP cells.
Ellfolk M, Norlin M, Gyllensten K, Wikvall K.
Department of Pharmaceutical Biosciences, University of Uppsala, Sweden.

In this study, we examined whether 1alpha,25-dihydroxyvitamin D(3) (calcitriol), phenobarbital, and the antiretroviral drug efavirenz, drugs used by patient groups with high incidence of low bone mineral density, could affect the 25-hydroxylase activity or expression of human 25-hydroxylases in dermal fibroblasts and prostate cancer LNCaP cells.

Fibroblasts express the 25-hydroxylating enzymes CYP2R1 and CYP27A1.

LNCaP cells were found to express two potential vitamin D 25-hydroxylases-CYP2R1 and CYP2J2.

The presence in different cells of nuclear receptors vitamin D receptor (VDR), pregnane X receptor (PXR), and constitutive androstane receptor (CAR) was also determined.

Phenobarbital suppressed the expression of CYP2R1 in fibroblasts and CYP2J2 in LNCaP cells.

Efavirenz suppressed the expression of CYP2R1 in fibroblasts but not in LNCaP cells.

CYP2J2 was slightly suppressed by efavirenz, whereas CYP27A1 was not affected by any of the two drugs.

Calcitriol suppressed the expression of CYP2R1 in both fibroblasts and LNCaP cells but had no clear effect on the expression of either CYP2J2 or CYP27A1.

The vitamin D(3) 25-hydroxylase activity in fibroblasts was suppressed by both calcitriol and efavirenz.

In LNCaP cells, consumption of substrate (1alpha-hydroxyvitamin D(3)) was used as indicator of metabolism because no 1alpha,25-dihydroxyvitamin D(3) product could be determined. The amount of 1alpha-hydroxyvitamin D(3) remaining in cells treated with calcitriol was significantly increased.

Taken together, 25-hydroxylation of vitamin D(3) was suppressed by calcitriol and drugs.

The present study provides new information indicating that 25-hydroxylation of vitamin D(3) may be regulated. In addition, the current results may offer a possible explanation for the impaired bone health after treatment with certain drugs.

PMID: 19286836 [PubMed - indexed for MEDLINE


This paper seems to confirm that hydroxylation of D3 is indeed downregulated by the VDR.

It seems that in the tissues, 25-Hydroxylation of D3 is done by different cyps, which is no surprise.

I am not sure what 1alpha-hydroxyvitamin D(3) is. It seems to me, this is just the D3 we know and 'love' ... ?

Frans



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Prof Trevor Marshall
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 Posted: Sat Aug 15th, 2009 11:52

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Frans,
I have not had to update the Figure 1, although I have been keeping an eye on it. I decided to omit CYP2R1, along with several other enzymes, because I was not happy with evidence for their equivalence to the primary enzymes.

The change in knowledge about the PXR over the last 18 months has had a huge impact on Figure 1. But the same in-vitro study which said PXR was activated by minocycline (a key piece of the scientific puzzle) also said Clindamycin did the same thing, something that I was unable to verify and which makes little sense based on our clinical observations.

Wet biology is an imprecise art, and as more and more orphan nuclear receptors are discovered, I suspect they will factor into the metabolism more than we can possibly imagine. So I am more interested in the overview, rather than enzyme substitution, at this point in time.
 


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