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Vitamin D Binding Protein: A Historic Overview.

Roger Bouillon1, Frans Schuit2, Leen Antonio1,3

  • 1Laboratory of Clinical and Experimental Endocrinology, Department of Chronic Diseases, Metabolism and Ageing, KU Leuven, Leuven, Belgium.

Frontiers in Endocrinology
|January 31, 2020
PubMed
Summary
This summary is machine-generated.

Vitamin D binding protein (DBP) transports vitamin D metabolites, preventing deficiency and maintaining calcium homeostasis. Despite low vitamin D levels in DBP-null individuals, bone health remains normal, supporting the free hormone hypothesis.

Keywords:
1,25-dihydoxyvitamin D25-hydoxyvitamin Dactinmegalinvitamin Dvitamin D binding protein (DBP)

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Background:

  • Vitamin D binding protein (DBP), also known as Group-specific Component (GC), is crucial for vitamin D metabolite transport.
  • DBP is evolutionarily ancient, belonging to the albuminoid family, and binds vitamin D metabolites with high affinity.
  • DBP also binds actin in higher vertebrates, preventing its polymerization, and is involved in fatty acid transport and immune function.

Purpose of the Study:

  • To elucidate the multifaceted roles of Vitamin D Binding Protein (DBP) in vitamin D transport, calcium homeostasis, and other physiological processes.
  • To investigate the implications of DBP's genetic polymorphism and its potential impact on health.
  • To highlight the necessity for standardizing DBP assays for further research.

Main Methods:

  • Review of existing literature on DBP structure, function, and evolution.
  • Analysis of data from DBP-null mice and humans regarding vitamin D metabolite levels and calcium/bone homeostasis.
  • Discussion of DBP's interaction with vitamin D metabolites, actin, and its role in renal reabsorption via megalin and cubilin.

Main Results:

  • DBP maintains a large circulating pool of 25OHD, preventing rapid vitamin D deficiency.
  • DBP null mice and humans exhibit extremely low vitamin D metabolite concentrations, yet maintain normal calcium and bone homeostasis.
  • DBP's role in preventing actin polymerization and its involvement in fatty acid transport and immunity were discussed.

Conclusions:

  • The 'free hormone hypothesis' is supported for the vitamin D hormone 1,25(OH)2D, as normal bone homeostasis is maintained despite low circulating levels in the absence of DBP.
  • DBP's genetic polymorphism (over 120 variants) has unclear health consequences, necessitating further investigation.
  • Standardization of DBP assays is critical for advancing research into DBP's physiological and pathological roles.