Abstract
Vitamin D is a micronutrient that plays a key role in phosphocalcic metabolism. The postmenopausal population presents a risk of deficiency in this vitamin due to hormonal alterations which, in the case of obesity, would be exacerbated. The objective was to assess the status of vitamin D in a postmenopausal population and determine the relationship of 25-hydroxivitamin D [25(OH)D] and its metabolites with anthropometric parameters. The study included 78 healthy postmenopausal women aged from 44 to 76. The nutrient intake assessment was carried out using the 24 h reminder (R24h). 25(OH)D was analyzed using ultra-high-performance liquid chromatography (UHPLC). A total of 80% and 68% of the women studied did not reach sufficient values of 25(OH)D and 25-hydroxivitamin D3 [25(OH)D3], respectively, which was inversely correlated with Body Mass Index (BMI) (r = −0.25, p = 0.04), hip perimeter (r = −0.26 and r = −0.24, all p < 0.05), arm circumference (r = −0.29, p = 0.01) and fat mass (r = −0.28 and r = −0.26, all p < 0.05). 25(OH)D3 is the metabolite that contributed most to this association. In conclusion, 25(OH)D3 levels are related to anthropometric parameters in the postmenopausal women in this study, confirming insufficient status in the majority of the population. Approach strategies are necessary to correct and avoid this risk in order to ensure future quality of life.
Highlights
Vitamin D is a fat-soluble vitamin that enters the body through exposing the skin to sunlight and through food and dietary supplement intake
The other anthropometric parameters are approximately within the reference values, they were more suitable in the group with the lowest Body Mass Index (BMI)
The population followed a slightly hyperproteic diet, and while the rest of the variables were within the reference values, except for vitamin D, levels were below the reference values in both groups (
Summary
Vitamin D is a fat-soluble vitamin that enters the body through exposing the skin to sunlight and through food and dietary supplement intake. For vitamin D to become biologically active, it must first be hydroxylated in the liver to 25-hydroxyvitamin D (25-OH-D), which is the metabolite used to assess a subject’s vitamin D status, and in the kidneys to 1,25-dihydroxyvitamin D (1,25-(OH)2 -D), which is its active form [1]. Due to nutritional deficits, liver and/or kidney failure, resistance to the action of vitamin D [3], and a low exposure to sunlight and the use of sunscreen [4]. The theory that genetics has an impact on vitamin D deficiency is gaining strength [5]. A vitamin D deficiency causes a decrease in the intestinal absorption of calcium (Ca), reducing its status and triggering the release of Parathyroid Hormone
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