Effects of Cholecalciferol on Key Components of Vitamin D-Endo/Para/Autocrine System in Experimental Type 1 Diabetes

Mazanova, Anna; Shymanskyi, Ihor; Lisakovska, Olha; Hajiyeva, Lala; Komisarenko, Iuliia; Veliky, M. M.

doi:10.1155/2018/2494016

Cited by 19 publications

(8 citation statements)

References 24 publications

(30 reference statements)

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“…Hence, insulin deficiency could possibly reduce the activity of these enzymes, leading to decreased levels of some of the vitamin D metabolites [ 26 , 27 , 28 ]. This hypothesis was supported by more recent studies [ 29 , 30 ]. However, no prospective controlled studies in humans evaluating a broad spectrum of vitamin D metabolites and related biochemical parameters have been performed to date.…”

Section: Introductionsupporting

confidence: 81%

Evaluation of Vitamin D Metabolism in Patients with Type 1 Diabetes Mellitus in the Setting of Cholecalciferol Treatment

et al. 2020

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In this prospective controlled study, we examined 25 adults with adequately controlled (HbA1c level < 8.0%) type 1 diabetes mellitus (T1DM) and 49 conditionally healthy adults, intending to reveal the diversity of vitamin D metabolism in the setting of cholecalciferol intake at a therapeutic dose. All patients received a single dose (150,000 IU) of cholecalciferol aqueous solution orally. Laboratory assessments including serum vitamin D metabolites (25(OH)D3, 25(OH)D2, 1,25(OH)2D3, 3-epi-25(OH)D3 and 24,25(OH)2D3), free 25(OH)D, vitamin D-binding protein (DBP) and parathyroid hormone (PTH) as well as serum and urine biochemical parameters were performed before the intake and on Days 1, 3 and 7 after the administration. The studied groups had no significant differences in baseline parameters except that the patients with diabetes showed higher baseline levels of free 25(OH)D (p < 0.05). They also lacked a correlation between the measured and calculated free 25(OH)D in contrast to the patients from the control group (r = 0.41, p > 0.05 vs. r = 0.88, p < 0.05), possibly due to the glycosylation of binding proteins, which affects the affinity constant for 25(OH)D. The elevation of vitamin D levels after the administration of cholecalciferol was comparable in both groups, with slightly higher 25(OH)D3 levels observed in the diabetes group throughout the study since Day 1 (p < 0.05). Overall, our data indicate that in patients with adequately controlled T1DM 25(OH)D3 levels and the therapeutic response to cholecalciferol is similar to that in healthy individuals.

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Section: Introductionsupporting

confidence: 81%

Evaluation of Vitamin D Metabolism in Patients with Type 1 Diabetes Mellitus in the Setting of Cholecalciferol Treatment

et al. 2020

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“…Vitamin D 3 exerts its biological effect mainly through VDR (vitamin D receptor), which belongs to the nuclear receptor superfamily and regulates gene expression in a ligand-dependent manner. Their discovery and synthesis in cells of "unconventional" organs and tissues for this vitamin implies a wider range of physiological effects of the vitamin [34,35].…”

Section: Resultsmentioning

confidence: 99%

Hepatic steatosis indices as predictors of vitamin D3 deficiency in patients with NAFLD associated with type 2 diabetes

Aludwan

Kobyliak

Abenavoli

et al. 2020

Clinical Diabetology

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Background. Recently, vitamin D 3 deficiency is consi dered one of the factors associated with the develop ment of nonalcoholic fatty liver disease (NAFLD). The aim was to evaluate steatosis indices and metabolic parameters in NAFLD depending on vitamin D 3 status. Methods. According to the recommendations of the European Society of Endocrinology, all patients were divided into 3 groups: group 1-with an optimal level of vitamin D 3 (30 ng/mL); group 2-vitamin D 3 insufficiency (21-29 ng/mL) and group 3-vitamin D 3 deficiency (< 20 ng/mL). Results. The study included 126 T2D patients with NAFLD diagnosed with ultrasound. The highest hepatic steatosis (HSI) and fatty liver (FLI) index values were diagnosed in vitamin D 3 deficiency as compared to optimal group (HSI-43.34 ± 6.59 vs. 39.67 ± 4.37; P = 0.032 and FLI-79.21 ± 19.61 vs. 64.96 ± 17.72; P = 0.007). Triglyceride and glucose index (TyG) also were insignificantly elevated parallel to vitamin D 3 status worsened (P = 0.175). In multivariate logistic re gression analysis all steatosis indices were independent from transaminases activity, body mass index (BMI) and T2D duration associated with vitamin D 3 deficiency. Conclusions. Hepatic steatosis indices (HSI, FLI and TyG) independently from anthropometric parameters and transaminase activity associated with D 3 deficiency in

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“…The data presented in Table show that diabetes causes a decrease in serum 25OHD level by 2.2 times compared with control mice. It may reflect the presence of severe vitamin D deficiency most likely due to inhibition of synthesis or/and enhanced catabolism of biologically active hydroxylated forms of vitamin D. In our previous works, we found essential changes in the functioning of vitamin D-metabolizing enzymes in liver tissue induced by T1D [16]. Vitamin D 3 supplementation partially normalized serum 25OHD without marked effect on blood glucose level (17.8 ± 3.9 mmol/l).…”

Section: Resultsmentioning

confidence: 73%

Vitamin D(3) regulates hepatic VEGF-A and apelin expression in experimental type 1 diabetes

Labudzynskyi¹,

Shymanskyi²,

Lisakovska³

et al. 2020

Ukr.Biochem.J

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The deficiency of vitamin D is associated with the risk of various chronic diseases, including diabetes mellitus and its complications. Given the strong genomic action of vitamin D hormone-active form, its deficiency can lead to dysfunction of cytokine signaling pathways, including those dependent on vascular endothelial growth factors (VEGFs) and apelin. The present study was carried out to define the link between VEGF-A and apelin expression in liver, hepatocytes viability and vitamin D status at experimental type 1 diabetes in mice. We established that chronic hyperglycemia at streptozotocin-induced diabetes was accompanied by a 2.2-fold decrease in 25OHD content in the serum and increased hepatocytes apoptosis and necrosis. Vitamin D deficiency correlated with increased apelin and VEGF-A (8-and 1.6-fold respectively) expression. Almost complete restoration of circulatory 25OHD content in serum was achieved at vitamin D 3 treatment (800 IU/kg, per os, for 2 months) followed by reduced apelin and VEGF-A expression in liver and the decline of hepatocytes apoptosis. We conclude that vitamin D 3 can be involved in cell survival, angiogenesis and fibrogenesis by modulating VEGF-A and apelin dependent regulatory systems in diabetic liver.

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Effects of Cholecalciferol on Key Components of Vitamin D-Endo/Para/Autocrine System in Experimental Type 1 Diabetes

Cited by 19 publications

References 24 publications

Evaluation of Vitamin D Metabolism in Patients with Type 1 Diabetes Mellitus in the Setting of Cholecalciferol Treatment

Evaluation of Vitamin D Metabolism in Patients with Type 1 Diabetes Mellitus in the Setting of Cholecalciferol Treatment

Hepatic steatosis indices as predictors of vitamin D3 deficiency in patients with NAFLD associated with type 2 diabetes

Vitamin D(3) regulates hepatic VEGF-A and apelin expression in experimental type 1 diabetes

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