jimmylegs wrote:Enhancement of vitamin D3 effect on bone metabolism in weanling rats orally administered zinc sulphate
The interaction of vitamin D3 and zinc on bone metabolism [bone, yes. Vitamin D?]was investigated in the femur of weanling rats. Oral administration of vitamin D3 (1.0 μg/100 g body weight) did not cause any increase in the zinc accumulation in the femoral tissue following treatment with zinc sulphate (1.0 mg Zn/100 g). Administration of vitamin D3 or zinc produced significant increases the alkaline phosphatase activity and DNA content of the femoral diaphvsis but not of the epiphysis. The increase in alkaline phosphatase activity was enhanced additionally by simultaneous administration of vitamin D3 and zinc. Moreover, the increase in DNA content was enhanced markedly (about 4 times) by these treatments. At a dose of 0.5 μg of vitamin D3 per 100 g, DNA content was at the control level. This level was increased about 2 times by simultaneous administration of zinc (1.0 mg/100 g).
jimmylegs wrote:The effect of toxic doses of cholecalciferol (vitamin D3) on the serum zinc levels in rats.
Zinc is a trace element important to bone mineralization as well as, in general, nutrition. It is known that cholecalciferol (vitamin D3) affects bone metabolism. In this study, toxic doses of vitamin D3 were injected subcutaneously (25 micrograms/d) to rats for 5 wk. It caused a significant increase in serum zinc levels (p < 0.02). On the other hand, no significant increase was detected in the other groups. Excessive amounts of vitamin D3 caused bone breakdown and increased the levels of zinc in blood.
NZer1 wrote:If Vit D is involved with parathyroid, thyroid, liver and kidneys, then the Thyroid connection to Thalamus, hypothalamus etc may be the link to dysautonomia and the Michael Arata focus on improvement from his 'treatment' approach might be as much about the signal transmission improvement as has been suggested because of the diet and Vit focus (with the wellness package) as well as the manual stimulation of the vagus nerve with PTA.
All together physically and chemically re-booting the autonomic nervous system?
jimmylegs wrote:The immunoregulatory function of vitamin D: implications in chronic kidney disease (2012)
http://www.nature.com/nrneph/journal/v8 ... 12.93.html
"Most of the biological actions of 1,25(OH) 2 D 3 are mediated through the vitamin D receptor (VDR)."
DIETARY REFERENCE INTAKES FOR Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc
http://www.nap.edu/openbook.php?record_ ... 6&page=443
"The structural role of zinc involves proteins that form domains capable of zinc coordination, which facilitates protein folding to produce biologically active molecules. The vast majority of such proteins form a “zinc finger-like” structure created by chelation centers, including cysteine and histidine residues (Klug and Schwabe, 1995). "
Zinc-induced conformational changes in the DNA-binding domain of the vitamin D receptor determined by electrospray ionization mass spectrometry
http://www.sciencedirect.com/science/ar ... 0597002298
"...the binding of the first Zn2+ ion to the protein results in very little conformational change in the protein. The binding of a second Zn2+ ion resulted in a significant alteration in the structure of the protein"
NZer1 wrote:Ed can you help me understand some thing please.
What is Vit D deficiency?
What is illness created hi use of Vit D?
Do the people with deficiency in Vit D actually have intake but not able to metabolise it?
I'm confused by the terms and head off with thoughts that maybe wrong at the start.
jimmylegs wrote:yes looks like we agree more science is needed.
would you agree that circulating levels of 25(OH)d3 from diet and sunshine would rely heavily on all the ingredients needed to effect hydroxylation?
I would hazard a guess that many other critical elements are involved in these pathways and severe deficiencies of any would cause problems if they involved the specific pathways that are needed for a particular reaction to occur.It is concluded that severe dietary Zn deficiency in rats caused a functional and structural impairment of liver microsomal P450 via a free radical medicated-like mechanism.
Enzymes involved in the activation and inactivation of vitamin D.
Prosser DE, Jones G.
Six cytochrome P450 (CYP) isoforms have been shown to hydroxylate vitamin D. Four of these, CYP27A1, CYP2R1, CYP3A4 and CYP2J3, are candidates for the enzyme vitamin D 25-hydroxylase that is involved in the first step of activation. The highly regulated, renal enzyme 25-hydroxyvitamin D-1alpha-hydroxylase contains the component CYP27B1, which completes the activation pathway to the hormonal form 1alpha,25-dihydroxyvitamin D(3). A five-step inactivation pathway from 1alpha,25-(OH)(2)D(3) to calcitroic acid is attributed to a single multifunctional CYP, CYP24A1, which is transcriptionally induced in vitamin D target cells by the action of 1alpha,25-(OH)(2)D(3). On the basis of alignments and crystal structures of other CYPs, homology models of vitamin-D-related CYPs have been generated. Two human forms of rickets caused by mutations of CYP2R1 and CYP27B1, as well as mouse knockout models of CYP27A1, CYP27B1 and CYP24A1, are helping us to establish the full in vivo physiological roles of the vitamin-D-related hydroxylases.
Anonymoose wrote:Maybe this has something to do with the zinc/vit d dilemna. Activation of renal NMDA receptors decreases vitamin d synthesis. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2980358/ Zinc inhibits NMDA receptors. http://www.jneurosci.org/content/18/16/6163.short and http://www.ncbi.nlm.nih.gov/pubmed/21504727 So, zinc supplementation blocks NMDA receptors (I think NMDA is an issue in MS) and allows for greater vitamin d synthesis?
Didn't have time to read through all of that so it might not fit at all.
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