Calcium Question

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Lests55

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So Vitamin D increases calcium and phosphate resorption of bones. Doesn't that mean bones are broken down? But, of course, Vit D is good for bones and you get osteomalacia, rickets, etc without them....:confused:

What am I missing?

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Does vitamin D cause increased resorption of bone? I don't think that's true, at best it's a gross oversimplification, I think it does stimulate osteoclasts, but this is really in order to increase formation of new bone. However, Vitamin D's main action is to increase gi absorption of calcium and phosphate, which provides the correct solubility product to mineralize bone. It also as a similar action in the kidney.
 
Agree with turkeyjerky. I just did a question in UW on this topic less than 10 minutes ago haha
 
Formation of normal osteoid is dependent on active Vit D. Without Vit D you get excess osteoid that is devoid of minerals. Remember to have strong bones you need to mineralize osteoid with Ca, PO4, hydroxide and bicarb to form hydroxyapatite.

Therefore, soft bones = bending and bowing of the legs = rickets.
 
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PTH is responsible for breakdown of bones in the way your thinking. Excess PTH can cause osteoporosis. Vitamin D is synergistic with PTH and stimulates the calcium pump on the osteoblast surface to move calicum out of bone fluid and into the extra cellular fluid.
Hope that helps
 
Vitamin D stimulates bone remodeling, but remember it's single-most important action is to increase GI reabsorption of calcium. It also increases renal retention of calcium.

Thus, your body will have more calcium overall.

Despite the fact that vitamin D actually causes calcium and phosphate to be drawn out of bone, the overall net effect is to build bone.
 
Associating vit. D with building and resorption of bone:

  1. Well, the main function of Vit. D is to maintain the appropriate conc. of serum calcium (sCa2+) and phosporus (sPO43-)
  2. Low [sCa2+] will activate PTH
  3. Both PTH (thus low sCa2+ indirectly) and low [sPO43-] will directly activate 25-hydroxycholealciferol 1-hydroxylase (aka alpha-1-hydroxylase) in kidney, converting the less active form of vit. D to its more potent 1,25-(OH)2 form
  4. 1,25-(OH)2 increases sCa2+ and sPO43-in 2 ways--mainly by increasing duodenal epithelial cell production of Ca2+ binding protein or by increasing osteoclast activities in the bone
  5. If there's adequate Ca2+ in the diet, sCa2+ level will quickly increase--far faster that breaking bones--to the point where the serum becomes slightly hypercalcemic
  6. The hypercalcemia will deactivate PTH rls and activate the rls of Calcitonin, which will inhibit osteoclast activities
  7. Thus, bone resorption is prevented if there's adequate Ca2+ in diet
  8. For someone who overdoses on vit. D, one of the consequences IS bone resorption--maybe by somehow knocking out the calcitonin activity??
  9. In terms of its effects on building bone matrix and preventing osteomalacia and rickets, vit. D binds to osteoblast receptors
  10. The binding stimulates the release of alkaline phosphatase, which will dephosphorylate pyrophosphate, promoting bone mineralization
  11. Another function of vit. D is to stimulate macrophage stem cell conversion into osteoclasts--maybe to help with renewing the bone matrix--mech. is still unknown
  12. Another postulation as to why vit. D deficiency leads to weakening of the bone is because of its effect on Ca2+ absorption. Hypocalcemia activates PTH, which will increase Ca2+ but decrease phosphorus absorption in the kidneys. The lack of phosphorous in the bone is the cause of improper mineralization of the bone (from big Robbins 7th ed.)
Sources: Lippincott Biochem vit D, Kaplan note biochem vit. D, RR Path vit. D, big Robbins 7th ed.

PS. just joined SDN... so pls excuse me if i don't know the proper forum etiquette :love:
 
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