Introduction In circulation, 99% vitamin D is transported by binding to vitamin D binding protein (VDBP) and albumin. Vitamin D at free form and vitamin D binding to albumin are defined as bioavailable vitamin D. Vitamin D deficiency is associated with atherogenic lipid profile and insulin resistance. Remnant cholesterol is defined as the cholesterol component of triglyceride-rich lipoproteins and contributes to the atherosclerotic burden. The aim of this study was to investigate the association between bioavailable vitamin D and remnant cholesterol in patients with type 2 diabetes mellitus (T2DM). Methods A total of 198 T2DM patients and 208 non-diabetic subjects underwent biochemical measurements of lipid profiles, 25(OH)D, VDBP, CRP and albumin levels. Their demographic characteristics (age, sex) were questioned. Subjects with thyroid, kidney and liver dysfunction and using lipid-lowering therapy were not included in the study. The diagnosis of T2DM was made according to the American Diabetes Association ADA 2016 criteria. Classification of vitamin D levels was done according to the Endocrine Society. Bioavailable vitamin D concentrations were calculated. Results High-density lipoprotein cholesterol (HDL), 25(OH)D, free vitamin D and bioavailable vitamin D levels were significantly lower in diabetic patients than in non-diabetic patients while triglyceride, remnant cholesterol and CRP levels were found to be significantly higher. VDBP was positively correlated with CRP and remnant cholesterol in diabetic patients, but not in non-diabetic patients. Cut-off values were determined from non-diabetics as 3.56 ng/mL for bioavailable vitamin D and 26.56 mg/dL for remnant cholesterol. Logistic regression analysis in the control group showed that the odds ratio for increasing remnant cholesterol above the cut-off value was determined as 2.01 for low bioavailable vitamin D and 1.1 for elevated CRP. However, in T2DM there was no significant relationship. In all subjects, low bioavailable vitamin D increased the remnant cholesterol above the cut-off by 2.18-fold independent of the presence of T2DM. However, there was no significant risk to increase remnant cholesterol, considering a total 25(OH) D deficiency in all groups. Conclusions Low bioavailable vitamin D was found to be a risk factor for elevated remnant cholesterol. This relationship was not detected in patients with T2DM. We believe that the inflammation observed in Diabetes Mellitus may increase the concentrations of VDBP and a decrease in bioavailable vitamin D levels. Therefore, measuring VDBP and calculating the bioavailable vitamin D may provide additional information about the actual vitamin D status.
In addition to its role in serum calcium homeostasis, the anti-tumor function of 1,25-dihydroxyvitamin D 3 (calcitriol) in cancer development is well established. N-myc Downstream Regulated Gene 2 which functions as a tumor suppressor gene has recently been shown to be downregulated in various cancer leading to increased tumor incidence, progression and metastasis. The goal of this study was to investigate the possible effects of calcitriol treatment on NDRG2 expression in BCPAP papillary thyroid carcinoma cells. Methods:The experiments were carried on human primary thyroid follicular epithelial cells (Nthy-ori-3-1), and human papillary thyroid carcinoma cells (BCPAP). The half maximal inhibitory concentration (IC 50 ) of calcitriol on BCPAP cells was determined by WST-1 assay. BCPAP cells were treated with 15 and 30µM calcitriol for 24, 48, and 72 hours, respectively. Basal NDGR2 expression in Nthy-ori-3-1 and BCPAP cells as well as the alterations on NDRG2 expression in calcitriol treated BCPAP cells were evaluated with western blot.Results: A significant downregulation of NDRG2 was observed in BCPAP cells when compared to Nthy-ori-3-1 cells (p<0.01). IC 50 dose of calcitriol was found to be 64, 54 and 43µM for 24, 48 and 72 hours, respectively. NDRG2 protein expression levels were significantly increased in 30µM calcitriol treated BCPAP cells after 48 hours (p<0.05).Conclusions: Calcitriol induced NDRG2 protein expression in BCPAP cells. We predict that calcitriol increased NDRG2 protein levels in BCPAP cells via c-Myc repression, which is upregulated by aberrant Wnt/β-catenin signaling. Further investigation is required to enlighten the possible effect mechanisms of calcitriol in BCPAP cells.
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