Chiu KC, Chu A, Go VLW, Saad MF. Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Am J Clin Nutr 79, 820-825

Division of Clinical Epidemiology and Preventive Medicine, Department of Medicine, University of California-Los Angeles School of Medicine, 924 Westwood Boulevard, Los Angeles, CA 90024, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 06/2004; 79(5):820-5.
Source: PubMed


Although the role of vitamin D in type 2 diabetes is well recognized, its relation to glucose metabolism is not well studied.
We investigated the relation of 25-hydroxyvitamin D [25(OH)D] concentrations to insulin sensitivity and beta cell function.
We enrolled 126 healthy, glucose-tolerant subjects living in California. Insulin sensitivity index (ISI) and first- and second-phase insulin responses (1stIR and 2ndIR) were assessed by using a hyperglycemic clamp.
Univariate regression analyses showed that 25(OH)D concentration was positively correlated with ISI (P < 0.0001) and negatively correlated with 1stIR (P = 0.0045) and 2ndIR (P < 0.0001). Multiple regression analyses confirmed an independent correlation between 25(OH)D concentration and ISI (P = 0.0007). No independent correlation was observed between 25(OH)D concentration and 1stIR or 2ndIR. However, an independent negative relation of 25(OH)D concentration with plasma glucose concentration was observed at fasting (P = 0.0258), 60 min (P = 0.0011), 90 min (P = 0.0011), and 120 min (P = 0.0007) during the oral-glucose-tolerance test. Subjects with hypovitaminosis D (<20 ng/mL) had a greater prevalence of components of metabolic syndrome than did subjects without hypovitaminosis D (30% compared with 11%; P = 0.0076).
The data show a positive correlation of 25(OH)D concentration with insulin sensitivity and a negative effect of hypovitaminosis D on beta cell function. Subjects with hypovitaminosis D are at higher risk of insulin resistance and the metabolic syndrome. Further studies are required to explore the underlying mechanisms.

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Available from: Ken Chiu, Jun 24, 2014
    • "visceral fat; CT, computer tomography ; DEXA, dual-energy X-ray absorptiometry; GIR, glucose infusion rates; HOMA, homeostasis model assessment; IR, insulin resistance; PCOS, polycystic ovary syndrome; T2DM, type 2 diabetes mellitus D deficiency (vitamin D <50 nmol/L) in 50% of women and 31% of men living at latitudes >35 degrees south, which includes Melbourne, the location of the current study [6]. Low vitamin D levels have been found in type 2 diabetes mellitus (T2DM) and correlate with obesity, pancreatic beta cell dysfunction , and insulin resistance (IR) and risk of developing T2DM [7] [8] [9] [10]. Supplementation of vitamin D has been shown to improve IR [11] and prevent T2DM [9]. "
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    ABSTRACT: Polycystic Ovary Syndrome (PCOS) is underpinned by IR. In PCOS, the relationships between vitamin D, adiposity and IR are unclear. We aim to explore these relationships in lean and overweight women with PCOS. This is a cross-sectional study conducted in a tertiary medical centre. Participants included 42 women with PCOS and 34 controls without PCOS. Vitamin D and metabolic markers were measured. Detailed body composition and gold standard hyperinsulinaemic euglycaemic clamps were performed. The main outcome measures were plasma levels of vitamin D, adiposity measures and glucose infusion rate (GIR). Vitamin D levels were lower in overweight women with PCOS compared with overweight controls (31.6 and 46.1 nmol/nmol respectively, p = 0.01). Vitamin D was not associated with IR after adjustment for confounders; however, there was a significant interaction between PCOS and % body fat. Further analysis by PCOS status revealed that vitamin D was associated with IR in the PCOS group (β coefficient 2.1, 95% CI 0.2-4.0, p = 0.03), but not in the non-PCOS group. Vitamin D is associated with IR in women with PCOS, but not in controls. Large intervention studies are needed to determine if vitamin D supplementation can improve IR in PCOS. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 08/2015; DOI:10.1002/mnfr.201500259 · 4.60 Impact Factor
    • "Various nutritional factors could also influence the protection of the β cell in LADA; one of them is vitamin D (vitD), due to its immunomodulatory properties and its regulation of calcium concentration [11]. Some cross-sectional studies have found a relationship between serum concentration of vitD and insulin resistance and secretion in healthy adults [12] [13] [14] and those with diabetes [15] [16]; moreover, a prospective study with healthy adults found the same relationship [17]. An association between vitD intake and insulin sensitivity in premenopausal women [18] has been reported as well as the incidence and prevalence of metabolic syndrome [19] [20] and T2DM [21]. "
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    ABSTRACT: This study aimed to evaluate the relationship between vitamin D (vitD) intake and serum concentrations and insulin secretion (assessed by C-peptide serum concentration)/insulin resistance (determined by estimated glucose disposal rate [eGDR]) in patients with latent autoimmune diabetes in adults (LADA) and type 2 diabetes (T2DM). C-peptide, serum vitD, lipid profile, insulin, glucose, and glycosylated hemoglobin (HbA1c) were assessed; vitD intake was determined; and eGDR was calculated. Groups were compared using the Student t or Mann-Whitney U test. Correlations were performed between insulin secretion, insulin resistance, and vitD, and linear regression models were adjusted for confounding variables. Of 107 patients included, age was 55.3 ± 11.84 years old, and time since diabetes diagnosis was 13.23 ± 5.96 years. There were significant intergroup differences in age, body mass index (BMI), hip measurements, glucose, and HbA1c. The correlation between vitD intake and C-peptide for the whole group was significant (r = 0.213; P = .032) as well as for vitD deficiency/sufficiency in T2DM (P = .042), whereas neither was significant in eGDR. After adjustment for age, HbA1c, disease progression, physical activity, solar exposure, sex, and BMI, vitD intake was only significant in T2DM (P = .028). In serum vitD, only the correlation between eGDR and vitD in T2DM was significant and intragroup when comparing vitD sufficiency. After adjustments, significance was lost. Patients with LADA had lower intake of vitD, poorer metabolic control, lower BMI, and younger age compared to T2DM patients. There was no association between serum vitD or vitD intake and insulin secretion when analyzed by group, although vitD intake was associated with insulin resistance in T2DM, but not LADA. Copyright © 2015. Published by Elsevier Inc.
    Nutrition research 06/2015; 35(8). DOI:10.1016/j.nutres.2015.05.019 · 2.47 Impact Factor
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    • "Some animal studies showed that knockout of the vitamin D receptor in diabetic mice was associated with severe albuminuria and glomerulosclerosis [32]. Alternatively, vitamin D might slow the progression of DN by improving insulin secretion, delaying destruction of b-islet cells, affecting osteocalcin and consequently assisting in glucose metabolism [4] [33] [34]. In addition, 1, 25(OH) 2 D 3 is known as a RAS inhibitor due to its negative regulatory effect on renin production [35]. "
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    ABSTRACT: Objective There has been a long history documenting the usage of different vitamin D derivatives as therapy for renal diseases. However, there is no comprehensive assessment of the relation between vitamin D deficiency and risk of diabetic nephropathy (DN). In addition, the effect of vitamin D supplementation on DN is still unclear. The aim of this meta-analysis was to assess these issues by pooling together the results from cross sectional studies and clinical trials. Methods A systematic literature search of PubMed, Scopus, and Google Scholar was conducted up to September 2014. For cross-sectional studies, odds ratio (OR) was used as a measure of the association between vitamin D status and risk of DN, and for clinical trials mean and standard deviation (SD) of the main outcome (urine albumin/creatinine ratio (UACR)) in intervention and placebo groups were considered for analysis. Results The final selected articles were published between 2009 and 2014. A total of 3700 and 219 patients were enrolled in observational and interventional studies, respectively. The pooled ORs from 6 cross-sectional studies was 1.80 (95% CI, 1.25 to 2.59; p=0.002) indicating a significant inverse association between serum vitamin D status and risk of nephropathy in diabetic patients. However, the pooled data of UACR levels in clinical trials suggested no significant change following vitamin D supplementation (17.98; 95% CI, -35.35 to 71.32, p=0.51). Conclusion This meta-analysis showed the higher risk of nephropathy in vitamin D deficient diabetic patients. Causality in this association was not supported by pooling together the results of available clinical trials following vitamin D supplementation
    Nutrition 05/2015; 31(10). DOI:10.1016/j.nut.2015.04.009 · 2.93 Impact Factor
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