Vitamin D Deficiency, Insulin Resistance and FGF-23
Condition: Vitamin D Deficiency
MeSH terms: Insulin Resistance; Vitamin D Deficiency
Study type: Interventional

Summary: 
      The purpose of this project is to determine if treating vitamin D deficiency decreases
      insulin resistance and improves insulin secretion in healthy volunteers. Additionally, this
      project will investigate if treating vitamin D deficiency affects a new phosphate-regulating
      hormone called FGF-23.
    

Detailed description: 
      Vitamin D deficiency or hypovitaminosis D, defined as serum 25 hydroxyvitamin D < or = 20
      ng/mL, is prevalent in several populations in the United States, specifically minorities and
      the elderly. Causes of vitamin D deficiency include lack of exposure to sunlight,
      malnutrition, and drugs that alter vitamin D metabolism and absorption.

      Vitamin D is an essential factor for many organ systems. Data suggest that vitamin D is
      required for normal insulin secretion by the pancreas. Specifically, animal studies
      demonstrate that treatment of vitamin D deficiency improves insulin secretion. In humans,
      there is less consensus about the impact of vitamin D deficiency on insulin resistance. In
      one study of middle-aged patients with Type 2 diabetes mellitus, no association was seen
      between serum 25 hydroxyvitamin D levels and a measure of insulin resistance. However, in a
      larger study of younger glucose tolerant subjects, serum 25 hydroxyvitamin D levels were
      associated with both insulin secretion and insulin resistance. These data suggest that
      treatment of vitamin D deficiency may delay or prevent the development of insulin resistance,
      and thus diabetes mellitus type 2. Repletion of this common vitamin deficiency could
      therefore have major public health implications for the prevention of diabetes mellitus.

      Fibroblast growth factor 23 (FGF-23) is a newly discovered phosphaturic hormone that is
      regulated by both dietary and serum phosphate. Hormonal regulation of FGF-23, however, is
      largely unknown. Recent data suggest that vitamin D plays an important role in the regulation
      of FGF-23. Some groups have shown that inactivation of the vitamin D receptor gene decreases
      serum FGF-23 levels in mice; administration of 1,25 dihydroxyvitamin D stimulates the
      transcription of the FGF-23 gene in vitro. Little is known, however, about the regulation of
      FGF-23 by vitamin D in humans.

      Phosphate is critical for bone mineralization, muscle function, signal transduction, and the
      creation and utilization of energy. Vitamin D deficiency can result in phosphate
      malabsorption, osteomalacia and increased risk of fractures. Enhanced understanding of the
      regulation of this new phosphate-regulating hormone, FGF-23, will advance the field of
      phosphate metabolism.
    

Intervention name(s): Ergocalciferol; Ergocalciferol placebo
Intervention type(s): Dietary Supplement; Dietary Supplement
Intervention description(s): Ergocalciferol 50000 international units once a week for 12 weeks; Ergocalciferol placebo once a week for 12 weeks
Intervention MeSH terms: Ergocalciferols; Vitamin D
Allocation: Randomized
Intervention model: Parallel Assignment
Masking: Triple (Participant, Care Provider, Investigator)
Primary purpose: Treatment
Keywords: Vitamin D; Vitamin D deficiency; Insulin resistance; Diabetes; Diabetes mellitus; FGF-23; FGF23; Phosphate