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Details for messenger / hormone: calcitriol

EndoNet ID: ENH00016

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  • calcitriol
  • 1,25-(OH)2D3
  • 1,25(OH)2D3
  • 1alpha,25-dihydroxy Vitamin D3
  • 1alpha,25-dihydroxyvitamin D3
  • calcitrol
  • 1alpha,25-2-vitamin D3
  • 1alpha,25-dihydroxycholecalciferol
  • 1alpha,25-(OH)2D3
  • (5Z,7E)-(1S,3R)-9,10-seco-5,7,10(19)-cholestatriene-1,3,25-triol

General information

  • 1alpha,25(OH)2D3 causes inhibition of the proliferation of osteoblasts, arrests their growth, and stimulates expression of specific markers. [1]
  • The CYP27B1 gene encodes 25-hydroxyvitamin D3-1-alpha-hydroxylase (1-alpha-(OH)ase), an enzyme in the renal proximal tubule that catalyzes the hydroxylation and metabolic activation of 25-hydroxyvitamin D3 into 1,25-dihydroxyvitamin D3.
  • Vitamin D seems to exert a protective effect against common cancers. [2]
  • Calcitriol had non-uniform effects on parathyroid function and bone remodelling in uraemic patients. [3]
  • 1Alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3) is a potent mediator of differentiation and maintenance of specific functions of osteoblasts. [4]
  • The 1 alpha,25-dihydroxyvitamin D3 (VD3)-dependent stimulation of osteocalcin (OC) and osteopontin (OP) gene transcription in bone tissue is mediated by interactions of trans-activating factors with distinct VD3-responsive elements (VDREs). [5]
  • Calcitriol, the hormonally active form of vitamin D3 is produced by a cascade of reactions, including photochemical D3 synthesis in the skin and subsequent hydroxylation at the C-25 atom in the liver and finally at C-1alpha position in the kidney. [6]
  • The ability of 1,25(OH)2D3 to inhibit growth and promote differentiation of a variety of cell types has suggested diverse functions in preventing cancers, modulating the immune system, and controlling various endocrine systems. [7]


Hormone function

  • homeostasis
    • ion flow control

    Chemical classification

    • hormone
      • not genome-encoded
        • sterol lipids
          • secosteroids


      KEGG C01673

      Links to other resources

      KEGG C01673
      LIPID MAPS LMST03020258
      LipidBank VVD0285
      • Anatomical structure: kidney

        • Calcidiol hydroxylates in kidneys into calcitriol. [8]
        • The PTH receptor in the kidneys activates mitochondrial vitamin D1 alpha-hydroxylase, leading to increased serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], which, in turn, is a potent inducer of intestinal calcium absorption and bone resorption. [9]

        Influenced by:

        • PTHR1
          in kidney
        • VDR
          in kidney
          • The synthesis of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) is most strongly regulated by dietary calcium and the action of parathyroid hormone to increase 1α-hydroxylase (1α-OHase) and decrease 24-hydroxylase (24-OHase) in kidney proximal tubules. [10]
          • 1,25-(OH)2D3 synthesis, induced by dietary calcium restriction, is also the result of negative feedback regulation blockade. [11]
          • Tissue-specific down-regulation of VDR by hypocalcemia blocks the 1,25-(OH)2D3 suppression of the 1α-OHase and upregulation of the 24-OHase in the kidney, causing a marked accumulation of 1,25-(OH)2D3 in the plasma. [11]
          • VDR clearly mediates the induction of the 24-OHase and the suppression of the 1α-OHase by 1,25-(OH)2D3. [12]
          • Thus, the PTH secreted under hypocalcemic conditions causes unbridled 1α-OHase activity in kidney and completely suppresses the 24-OHase activity causing high levels of 1,25-(OH)2D3 in the circulation. [13]
          • The accumulation of 1,25-(OH)2D3 in the plasma is because of high rates of production and an absence of renal degradation. This impressive regulation only serves to ensure high rates of calcium mobilization from bone as needed for soft tissue needs such as growth as shown by bone ash and skeletal density determinations. [11]
          • Loss of renal VDR interferes with the otherwise normal ability of 1,25-(OH)2D3 to exert negative feedback suppression on 1α-OHase. It, therefore, appears that the basis of this regulatory series of events rests with the regulation of VDR expression in renal and perhaps parathyroid cells by ambient calcium concentrations. [11]


      beta cell of islet of Langerhans Present
      • insulin
      bone Present
      • tumor-induced osteomalacia
      • autosomal dominant hypophosphatemic rickets
      • X-linked hypophosphatemic rickets
      • osteoporosis
      • FGF-23
      chief cell of parathyroid gland Present
      • PTH
      hematopoietic stem cell Present
      • RANKL
      hepatocyte Present
      • negative regulation of bile acid biosynthetic process
      keratinocyte Present
      • cathelicidin
      kidney Present
      • phosphate ion homeostasis
      • Secondary hyperparathyroidism
      • calcitriol
      macrophage Present
      • negative regulation of macrophage derived foam cell differentiation
      osteoblast Present
      • regulation of gene expression
      • alopecia
      • mineral metabolism
      • rickets
      • TGF-beta 2
      • RANKL
      • FGF-23