Article

Low Serum 25-Hydroxyvitamin D Is Associated with Increased Risk of the Development of the Metabolic Syndrome at Five Years: Results from a National, Population-Based Prospective Study (The Australian Diabetes, Obesity and Lifestyle Study: AusDiab)

Centre hospitalier Universitaire de Québec, Centre hospitalier de l'Université Laval, Laval University, 2705 Boulevard Laurier, Québec, Canada G1V 4G2.
The Journal of Clinical Endocrinology and Metabolism (Impact Factor: 6.31). 03/2012; 97(6):1953-61. DOI: 10.1210/jc.2011-3187
Source: PubMed

ABSTRACT Serum 25-hydroxyvitamin D [25(OH)D] concentration has been inversely associated with the prevalence of metabolic syndrome (MetS), but the relationship between 25(OH)D and incident MetS remains unclear.
We evaluated the prospective association between 25(OH)D, MetS, and its components in a large population-based cohort of adults aged 25 yr or older.
We used baseline (1999-2000) and 5-yr follow-up data of the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab).
Of the 11,247 adults evaluated at baseline, 6,537 returned for follow-up. We studied those without MetS at baseline and with complete data (n = 4164; mean age 50 yr; 58% women; 92% Europids).
We report the associations between baseline 25(OH)D and 5-yr MetS incidence and its components, adjusted for age, sex, ethnicity, season, latitude, smoking, family history of type 2 diabetes, physical activity, education, kidney function, waist circumference (WC), and baseline MetS components.
A total of 528 incident cases (12.7%) of MetS developed over 5 yr. Compared with those in the highest quintile of 25(OH)D (≥34 ng/ml), MetS risk was significantly higher in people with 25(OH)D in the first (<18 ng/ml) and second (18-23 ng/ml) quintiles; odds ratio (95% confidence interval) = 1.41 (1.02-1.95) and 1.74 (1.28-2.37), respectively. Serum 25(OH)D was inversely associated with 5-yr WC (P < 0.001), triglycerides (P < 0.01), fasting glucose (P < 0.01), and homeostasis model assessment for insulin resistance (P < 0.001) but not with 2-h plasma glucose (P = 0.29), high-density lipoprotein cholesterol (P = 0.70), or blood pressure (P = 0.46).
In Australian adults, lower 25(OH)D concentrations were associated with increased MetS risk and higher WC, serum triglyceride, fasting glucose, and insulin resistance at 5 yr. Vitamin D supplementation studies are required to establish whether the link between vitamin D deficiency and MetS is causal.

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    • "Recent epidemiological, observational and interventional studies of elderly adults [14] [15] [16] [17], young adults [18], and children [19– 22] have suggested that low levels of serum 25-hydroxy vitamin D (25(OH)D), the recognized indicator of total vitamin D status in the body, are linked with some components of metabolic syndrome (MetS) like insulin resistance, obesity, dyslipidemia and hypertension . MetS predisposes to increased risk for diabetes, cardiovascular events and some other chronic diseases. "
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    ABSTRACT: Vitamin D deficiency is a common worldwide problem. Low levels of serum 25-hydroxy vitamin D [25(OH)D], as a marker of vitamin D deficiency, have been linked to a wide field of health problems, including metabolic diseases such as insulin resistance, type 1 and type 2 DM. There is no universal definition for cutoff value of vitamin D deficiency and it seems that it varies in different populations. Most previous studies have used a start rise of PTH as a criteria to detect threshold of serum 25(OH)D, However, the aim of this study was to determine a cutoff point of serum 25(OH)D for vitamin D deficiency based on HOMA-IR. Two hundred and ninety seven healthy children (aged 7-11 years) were enrolled. Serum 25(OH)D and PTH were measured and HOMA-IR was calculated. The ROC curve was utilized to obtain a cutoff of vitamin D deficiency based on HOMA-IR. 25(OH)D concentrations were inversely correlated with HOMA-IR levels (Spearman's r=-0.14, p=0.016). Serum 25(OH)D cutoff point was 11.6ng/mL (29nmol/L) in relation with HOMA-IR >2.1. By using this cutoff value, the prevalence of vitamin D deficiency was 43.4% in this study population of healthy children. We found that serum 25(OH)D levels are inversely associated with insulin resistance. These results suggest that in MetS patients it may benefit to determine cutoff value of 25(OH)D levels based on HOMA-IR.
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    • "The Promise (PROspective Metabolism and ISlet cell Evaluation) study supported the potential role of vitamin D in the pathogenesis of T2D, showing that higher 25[OH]D concentrations were independently associated with better beta-cell function and insulin sensitivity (Kayaniyil et al., 2011). Furthermore, the AusDiab (The Australian Diabetes, Obesity and Lifestyle) study further supported the hypothesis that hypovitaminosis D plays an important role in insulin resistance (Gagnon et al., 2012). It is not surprising, therefore, that the evolution of pre-diabetes to full-blown T2D may be reduced by 25% for every 10 nmol/l increase in 25[OH]D concentration (Deleskog et al., 2012). "
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    Journal of diabetes and its complications 11/2012; DOI:10.1016/j.jdiacomp.2012.10.005 · 1.93 Impact Factor
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    ABSTRACT: Recent compelling evidence suggests a role of vitamin D deficiency in the pathogenesis of insulin resistance and insulin secretion derangements, with a consequent possible interference with type 2 diabetes mellitus. The mechanism of this link is incompletely understood. In fact, vitamin D deficiency is usually detected in obesity in which insulin resistance is also a common finding. The coexistence of insulin resistance and vitamin D deficiency has generated several hypotheses. Some cross-sectional and prospective studies have suggested that vitamin D deficiency may play a role in worsening insulin resistance; others have identified obesity as a risk factor predisposing individuals to exhibit both vitamin D deficiency and insulin resistance. The available data from intervention studies are largely confounded, and inadequate considerations of seasonal effects on 25(OH)D concentrations are also a common design flaw in many studies. On the contrary, there is strong evidence that obesity might cause both vitamin D deficiency and insulin resistance, leaving open the possibility that vitamin D and diabetes are not related at all. Although it might seem premature to draw firm conclusions on the role of vitamin D supplementation in reducing insulin resistance and preventing type 2 diabetes, this manuscript will review the circumstances leading to vitamin D deficiency and how such a deficiency can eventually independently affect insulin sensitivity.
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