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Vitamin D Supplementation Reduces Renin-Angiotensin System Activity in Obesity

2014-08-27 03:15:55 | BioPortfolio

Summary

Hypothesis: Vitamin D supplementation lower renin-angiotensin system activity in obesity.

Specific Aim: To investigate whether Vitamin D supplementation in obesity improves the vascular sensitivity to angiotensin II.

Description

Vitamin D deficiency and obesity are international epidemics that have both been associated with increased activity of the renin-angiotensin system (RAS). Because increased RAS activity is associated with cardiovascular disease, interventions to lower RAS will have favorable public health impacts.

This study aims to evaluate whether the supplementation of Vitamin D in obese subjects will lower local tissue RAS activity. RAS activity will be evaluated by cross-sectional measurement of RAS components and by quantifying the vascular response to an infusion of angiotensin II. Subjects will be studied while Vitamin D deficient, and will return for repeat study following Vitamin D supplementation, for comparison.

Study Design

Allocation: Non-Randomized, Control: Uncontrolled, Intervention Model: Crossover Assignment, Masking: Open Label

Conditions

Obesity

Intervention

Vitamin D (ergocalciferol)

Location

Brigham and Women's Hospital
Boston
Massachusetts
United States
02115

Status

Recruiting

Source

Brigham and Women's Hospital

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:15:55-0400

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Medical and Biotech [MESH] Definitions

A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.

A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)

OXIDOREDUCTASES which mediate vitamin K metabolism by converting inactive vitamin K 2,3-epoxide to active vitamin K.

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A family of phylloquinones that contains a ring of 2-methyl-1,4-naphthoquinone and an isoprenoid side chain. Members of this group of vitamin K 1 have only one double bond on the proximal isoprene unit. Rich sources of vitamin K 1 include green plants, algae, and photosynthetic bacteria. Vitamin K1 has antihemorrhagic and prothrombogenic activity.

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