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Effect of a Single Colecalciferol Dose on Insulin Resistance

2014-08-27 03:15:41 | BioPortfolio

Summary

A Prospective Double-Blinded, Placebo Controlled, Randomized Trial comparing a single dose of Vitamin D (Colecalciferol) 300.00UI to placebo on patients with insulin resistance. Primary Outcome: Blood glucose and homeostasis model assessment for insulin resistance (HOMA-R) after 90 days. Study hypothesis: Vitamin D treatment may improve insulin resistance and decrease glucose level, since there is an association between hypovitaminosis D and increased insulin resistance.

Study Design

Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator), Primary Purpose: Treatment

Conditions

Insulin Resistance

Intervention

Colecalciferol (Vitamin D3) 300.000 UI, Placebo

Location

Hospital de Clínicas de Porto Alegre
Porto Alegre
Rio Grande do Sul
Brazil
90035-903

Status

Enrolling by invitation

Source

Hospital de Clinicas de Porto Alegre

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:15:41-0400

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Medical and Biotech [MESH] Definitions

A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.

Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS. It can be caused by the presence of INSULIN ANTIBODIES or the abnormalities in insulin receptors (RECEPTOR, INSULIN) on target cell surfaces. It is often associated with OBESITY; DIABETIC KETOACIDOSIS; INFECTION; and certain rare conditions. (from Stedman, 25th ed)

THIAZOLES with two keto oxygens. Members are insulin-sensitizing agents which overcome INSULIN RESISTANCE by activation of the peroxisome proliferator activated receptor gamma (PPAR-gamma).

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Rare autosomal recessive syndrome of extreme insulin resistance due to mutations in the binding domain of INSULIN RECEPTOR. Clinical features include severe intrauterine and postnatal growth restriction, characteristic dysmorphic FACIES; HIRSUTISM; VIRILIZATION; multiple endocrine abnormalities, and early death.

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