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The intestinal calcistat.

M K Garg1

  • 1Department of Endocrinology, Command Hospital (Southern Command), Pune, Maharashtra, India.

Indian Journal of Endocrinology and Metabolism
|November 20, 2013
PubMed
Summary
This summary is machine-generated.

Vitamin D deficiency (VDD) may not always cause clinical disease. Subclinical VDD, characterized by normal parathyroid hormone (PTH) and bone mineral density (BMD), may exist and requires further study.

Keywords:
Bone mineral densitycalciumphosphatase and parathormonevitamin D

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Area of Science:

  • Endocrinology
  • Nutritional Science
  • Bone Metabolism

Background:

  • Vitamin D is crucial for calcium homeostasis and bone health, primarily through its influence on calcium absorption and the parathyroid gland.
  • Vitamin D deficiency (VDD) is typically defined by serum 25-hydroxy vitamin D (25OHD) levels below 20 ng/ml.
  • The clinical manifestation of VDD varies, suggesting underlying regulatory mechanisms beyond systemic adaptation.

Purpose of the Study:

  • To investigate the existence of an intestinal calcistat that regulates calcium absorption independently of parathyroid hormone (PTH) levels.
  • To determine if all subjects with VDD exhibit clinical disease, such as secondary hyperparathyroidism or decreased bone mineral density (BMD).
  • To propose a new classification for subclinical VDD and identify early indicators.

Main Methods:

  • Hypothesized an intestinal calcistat involving the calcium-sensing receptor (CaSR) on intestinal brush border and the intestinal vitamin D system.
  • Described the proposed mechanisms of local adaptation (CaSR dampening active vitamin D metabolite generation, facilitating passive calcium absorption).
  • Outlined systemic adaptations (increased PTH, active vitamin D metabolites) in response to VDD and local adaptation failure.

Main Results:

  • Not all individuals with VDD develop secondary hyperparathyroidism or decreased BMD, indicating varying degrees of clinical manifestation.
  • Proposed that an increase in PTH and a decrease in BMD are the initial indicators of VDD, contingent on its duration.
  • Suggested that subjects with VDD but normal PTH and BMD should be classified as having subclinical VDD.

Conclusions:

  • An intestinal calcistat may regulate calcium absorption locally, influencing the systemic response to Vitamin D deficiency.
  • Elevated PTH and reduced BMD are suggested as the earliest signs of VDD, not universally present in all deficient individuals.
  • The concept of subclinical VDD is introduced for individuals with any degree of VDD but normal PTH and BMD, warranting further research into supplementation benefits.