Vitamin D

Vitamin D is not a true vitamin in many respects
Production of Vitamin D
Metabolism of Vitamin D
Functions of Vitamin D
Dietary Sources of Vitamin D

I.  Vitamin D is not a true vitamin in many respects:

  1. Only required from the diet under certain conditions
  2. Is normally produced in animal tissues
  3. Not generally produced by plants and microorganisms
  4. Its mechanism of action is essentially that of a steroid hormone
    1. The active metabolite is elaborated by one organ but acts on other target organs
    2. A feedback mechanism exists for controlling the rate of synthesis and secretion of the active metabolite

II.  Chemistry

  1. Several forms of vitamin D exist; nearly all arise from irradiation of sterols that are provitamins or precursors of the vitamin
  2. Most important forms:
    1. Ergocalciferol (vitamin D2). Produced when ergosterol, which occurs in plants, is activated by sunlight
    2. Cholecalciferol (vitamin D3). Produced when 7-dehydrocholesterol, found in animal epidermal cells, is activated by sunlight
    3. Ergocalciferol differs from cholecalciferol only by a double bond at the 22, 23 position and a methyl group at file 24 position
    4. Vitamin D2 and D3 possess equal activity for most mammalian species but ergoealciferol is only 1/10 as potent as cholecalciferol for chickens
  3. Vitamin D is not affected by oxidation or temperatures below 140°C and is stable in alkaline but not acid solutions

III.  Production of Vitamin D

  1. Ergosterol is the predominant provitamin in plants
    1. Converted to ergocalciferol (D2) by UV radiation
    2. Plant foods used in human diet essentially devoid of ergocalciferol
    3. 3Sun-cured hay contains significant amounts
  2. Cholesterol is the principle sterol of higher animals. Nearly every cell has capacity to synthesize cholesterol
    1. Squalene synthesized from acetate
    2. Converted to cholesterol then 7-dehydrocholesterol
    3. 7-dehydro cholesterol converted to cholecalciferol (D3) by UV light
    4. Released to vitamin D binding protein in plasma for transport, distribution and storage

IV.  Metabolism of Vitamin D

  1. Absorbed in small intestine
  2. Absorption is similar to fat absorption and facilitated by presence of fat and bile salts
  3. Vitamin D becomes associated with specific transport proteins
  4. Transported to liver via lymph system (as are triglycerides and cholesterol)
  5. Released in the liver to a specific vitamin D binding protein
  6. Part of vitamin D is 25-hydroxylated in the liver
  7. Activated to 1,25(OH)2D ,by the kidney in response to changes in blood Ca
  8. Rest is stored in fat tissue for future use
  9. After activation, the vitamin is metabolized and excreted via the bile

V.  Functions of Vitamin D

  1. Only clearly defined function of vitamin D is maintenance of Ca homeostasis in conjunction with PTH
    1. When blood Ca concentrations begin to fall, amounts of PTH increase
    2. This causes activation of 25(OH)D by hydroxylation of C-1 forming 1,25(OH)2D
    3. This has three effects:
      1. Signals cells of intestinal mucosa to increase Ca and P absorption
      2. There is an inunediate flux of Ca2+ from bone to plasma
      3. It signals distal kidney tubules to retain (resorb) more Ca
    4. Effects are thought to occur at least partly, through steroid hormone like mechanism which induces increased transcription and thus translation of mRNA's coding for proteins involved in absorption of Ca and P
      1. The steroid vitamin crosses the cell membrane and binds to cytosol receptor proteins
      2. Activation of this complex within cytosol allows its entry into the nucleus and binding to chromatin
      3. This results in increased formation and transfer into cytosol of mRNA for Ca and P transport proteins
      4. This enhances rate of synthesis of proteins involved in Ca and P absorption or resorption
  2. Receptors for 1,25(OH)2D are found in cells of other tissue (including pancreas and skin) so vitamin D may have other, as yet undiscovered functions
  3. Because kidney activation of the vitamin-hormone is central to its action and regulation of blood Ca, loss of kidney function will produce hypocalcemia and bone disease

VI.  Dietary Sources of Vitamin D

  1. Fish oils and egg yolks
  2. Milk and other supplemented processed foods
  3. Raw foodstuffs contain little or no vitamin D

VII.  Deficiency

  1. Deficiency results from:
    1. Insufficient vitamin production
    2. Dietary lack
    3. Malabsorption of fats
  2. Levels of PTH are increased, which enhance urinary excretion of phosphorus and further reduce bone calcification
  3. Deficiency symptoms
    1. Rickets
      1. Appears during growing period (children)
      2. Poor calcification of bones
      3. Poor cartilage cell growth
      4. Deformities of bones
    2. Blood changes
      1. Serum 25(OH)D3 below 5 ng/ml (normal levels are 30 mg/ml in US and 20 ng/ml in Europe)
      2. Decreased serum Ca and P
      3. Increased serum alkaline phosphatic
    3. Osteomalacia
      1. Occurs in adults
      2. Bone reabsorption weakens bone
      3. May occur with failure to absorb fat and fat soluble vitamins
      4. Chronic renal failure causes a problem

VIII.  Toxicity

  1. 10 times the RDA
  2. Symptoms
    1. Hypercalcemia (Ca> 12mg/dl) (also caused by hyperparathyroidism)
    2. Deposition of Ca in soft tissues (kidney, heart, lung, vasculature)
      1. Hypercalcuria, possibly stones
      2. Cardiac myopathy and afilerosclerotic lesions
      3. Melanin in the skin may protect man from vitamin D toxicity
      4. Exposure to equatorial versus Boston sunlight doubles the initial rate of pre-D3 production
      5. With increased exposure, previtamin D3 production decreased and increasing proportions of biologically inactive forms (lumisterol) were produced

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