Vitamin D insufficiency, preterm delivery and preeclampsia in women with type 1 diabetes - an observational study

Abstract Objectives Vitamin D plays an immunoregulatory activity. The aim of this study was to assess the correlation between blood serum 25(OH)D levels and Th17 and Treg circulating subsets, mainly Treg/inducible costimulatory-positive (ICOS+), which seems to have a protective role in autoimmunity, in children with type 1 diabetes mellitus (T1D) and their healthy siblings (S). The secondary aim was to evaluate the impact of vitamin D supplementation on these subsets. Patients and Methods 22 T1D and 33 S were enrolled. Glucose, hemoglobin A1c, 25 OH vitamin D (25[OH]D), T helper type 17 (Th17; CD4+CCR6+), regulatory T cells (Treg; CD4+CD25+Foxp3+), and Treg/ICOS+ cells were evaluated. According to human leukocyte antigen (HLA) haplotypes, subjects were classified as “at risk” (HLA+), “protective haplotypes” (HLA−; “nested controls”), and “undetermined” (HLAUND). T1D and S subjects were supplemented with cholecalciferol 1000 IU/die and evaluated after 6 months. Results Vitamin D insufficiency (74.4%) and deficiency (43%) were frequent. S subjects with 25(OH)D levels <25 nmol/L had Th17, Treg (p < 0.01), and Treg/ICOS+ (P < 0.05) percentages higher than subjects with 25(OH)D >75 nmol/L. Treg/ICOS+ percentages (P < 0.05) were higher in HLA− S subjects compared to percentages observed in S with T1D. At baseline, in S subjects, a decreasing trend in Th17 and Treg/ICOS+ values (P < 0.05) from vitamin D deficiency to sufficiency was observed; 25(OH)D levels were negative predictors of Treg/ICOS+ (R2 = 0.301) and Th17 percentages (R2 = 0.138). After 6 months, supplemented S subjects showed higher 25(OH)D levels (P < 0.0001), and lower Th17 (P < 0.0001) and Treg/ICOS+ (P < 0.05) percentages than at baseline; supplemented T1D patients only had a decrease in Th17 levels (P < 0.05). Conclusion Serum 25(OH)D levels seem to affect Th17 and Treg cell subsets in S subjects, consistent with its immunomodulating role. HLA role should be investigated in a larger population.

Download Full-text

Calcium Insufficiency Accelerates Type 1 Diabetes in Vitamin D Receptor-Deficient Nonobese Diabetic (NOD) Mice

Endocrinology ◽

10.1210/en.2011-1074 ◽

2011 ◽

Vol 152 (12) ◽

pp. 4620-4629 ◽

Cited By ~ 9

Author(s):

John P. Driver ◽

Deanna J. Lamont ◽

Conny Gysemans ◽

Chantal Mathieu ◽

David V. Serreze

Keyword(s):

Vitamin D ◽

Type 1 Diabetes ◽

Vitamin D Receptor ◽

Calcium Absorption ◽

Nod Mice ◽

Vitamin D Insufficiency ◽

Vitamin D Supplementation ◽

Chow Diet ◽

Β Cells

Vitamin D exerts important regulatory effects on the endocrine and immune systems. Autoimmune type 1 diabetes (T1D) development in the inbred NOD mouse strain can be accelerated by vitamin D insufficiency or suppressed by chronic treatment with high levels of 1α,25-dihydroxyvitamin D3. Consequently, a report that T1D development was unaffected in NOD mice genetically lacking the vitamin D receptor (VDR) was unexpected. To further assess this result, the mutant stock was imported to The Jackson Laboratory, backcrossed once to NOD/ShiLtJ, and progeny rederived through embryo transfer. VDR-deficient NOD mice of both sexes showed significant acceleration of T1D. This acceleration was not associated with alterations in immune cells targeting pancreatic β-cells. Rather, the capacity of β-cells to produce and/or secrete insulin was severely impaired by the hypocalcaemia developing in VDR-deficient NOD mice fed a standard rodent chow diet. Feeding a high-lactose calcium rescue diet that circumvents a VDR requirement for calcium absorption from the intestine normalized serum calcium levels, restored β-cell insulin secretion, corrected glucose intolerance, and eliminated accelerated T1D in VDR-deficient NOD mice. These findings suggest that calcium and/or vitamin D supplementation may improve disease outcomes in some T1D-prone individuals that are calcium deficient.

Download Full-text

Vitamin D Deficiency Likely in Youths With Type 1 Diabetes

Pediatric News ◽

10.1016/s0031-398x(09)70008-6 ◽

2009 ◽

Vol 43 (1) ◽

pp. 4

Author(s):

HEIDI SPLETE

Keyword(s):

Vitamin D ◽

Type 1 Diabetes ◽

Vitamin D Deficiency

Download Full-text

Levels of 25(OH)vitamin D in children and adolescents with type 1 diabetes mellitus and in healthy controls in Bulgarian population

Bone Abstracts ◽

10.1530/boneabs.2.p199 ◽

2013 ◽

Author(s):

Slavcheva Olga ◽

Konstantinova Maia ◽

Tsekova Adelina ◽

Savova Radka ◽

Arshinkova Margarita

Keyword(s):

Diabetes Mellitus ◽

Vitamin D ◽

Type 1 Diabetes ◽

Type 1 Diabetes Mellitus ◽

Children And Adolescents ◽

Healthy Controls ◽

25 Oh Vitamin D ◽

Bulgarian Population

Download Full-text

Genetic susceptibility to type 1 diabetes: genomic variants in the vitamin D pathway

Endocrine Abstracts ◽

10.1530/endoabs.59.p057 ◽

2018 ◽

Author(s):

Joana Almeida ◽

Dircea Rodrigues ◽

Franscisco Carrilho ◽

Joana Guimaraes ◽

Manuel C Lemos

Keyword(s):

Vitamin D ◽

Type 1 Diabetes ◽

Genetic Susceptibility ◽

Genomic Variants

Download Full-text

Vitamin D status and bone metabolism in adult patients with Type 1 diabetes mellitus

Endocrine Abstracts ◽

10.1530/endoabs.63.p614 ◽

2019 ◽

Author(s):

Eleftheria Barmpa ◽

Spyros Karamagiolis ◽

Stelios Tigas ◽

Georgios N Koukoulis ◽

Alexandra Bargiota

Keyword(s):

Diabetes Mellitus ◽

Vitamin D ◽

Type 1 Diabetes ◽

Type 1 Diabetes Mellitus ◽

Bone Metabolism ◽

Adult Patients ◽

Vitamin D Status

Download Full-text

Diabetes and osteoporosis

Orvosi Hetilap ◽

10.1556/oh.2011.29154 ◽

2011 ◽

Vol 152 (29) ◽

pp. 1161-1166 ◽

Cited By ~ 4

Author(s):

Zsuzsanna Valkusz

Keyword(s):

Vitamin D ◽

Type 1 Diabetes ◽

Bone Mass ◽

Fragility Fractures ◽

Vitamin D Supplementation ◽

Bone Collagen ◽

Skeletal Changes ◽

Glucagon Like Peptide 1 ◽

Bone Quantity

Over the last decades a considerable amount of data has accumulated to indicate that metabolic and endocrine alterations of diabetes affect bone quantity and quality. These skeletal changes may increase the risk of bone fracture. There is strong evidence that in type 1 diabetes the decreased bone mass, lack of insulin and insulin-like growth factor-1, dysregulation of adipokines, and increased levels of proinflammatory cytokines are in the background of fragility fractures. In type 2 diabetes hyperinsulinemia, insulin resistance and increased body weight may result in an increase of bone mass; however, accumulation of advanced glycation end products within the bone collagen driven by glucotoxicity may increase the cortical porosity. There is a higher incidence of falls resulting from diabetes-related co-morbidities such as diabetic retinopathy, peripheral neuropathy, hypoglycemic episodes and sometimes from the medications. Vitamin D deficiency has special impact on glucose metabolism and the prevalence of diabetes. Vitamin D supplementation in childhood can decrease incidence of type 1 diabetes by 80%. The effect of thiazolidinediones, glucagon-like peptide-1 agonists and metformin, agents for treatment of diabetes open a new connection between bone, carbohydrate and fat metabolism. Orv. Hetil., 2011, 152, 1161–1166.

Download Full-text