• The Korean Journal of Physiology and Pharmacology
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• v.14 no.3
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• pp.169-176
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• 2010

The hyperosmotic stimulus is regarded as a mechanical factor for bone remodeling. However, whether the hyperosmotic stimulus affects $1{\alpha}$, 25-dihydroxyvitamin $D_3$ ($1{\alpha},25(OH)_2D_3$)-induced osteoclastogenesis is not clear. In the present study, the effect of the hyperosmotic stimulus on $1{\alpha},25(OH)_2D_3$-induced osteoclastogenesis was investigated in an osteoblast-preosteoclast co-culture system. Serial doses of sucrose were applied as a mechanical force. These hyperosmotic stimuli significantly evoked a reduced number of $1{\alpha},25(OH)_2D_3$-induced tartrate-resistant acid phosphatase-positive multinucleated cells and $1{\alpha},25(OH)_2D_3$-induced bone-resorbing pit area in a co-culture system. In osteoblastic cells, receptor activator of nuclear factor ${\kappa}B$ ligand (RANKL) and Runx2 expressions were down-regulated in response to $1{\alpha},25(OH)_2D_3$. Knockdown of Runx2 inhibited $1{\alpha},25(OH)_2D_3$-induced RANKL expression in osteoblastic cells. Finally, the hyperosmotic stimulus induced the overexpression of TonEBP in osteoblastic cells. These results suggest that hyperosmolarity leads to the down-regulation of $1{\alpha},25(OH)_2D_3$-induced osteoclastogenesis, suppressing Runx2 and RANKL expression due to the TonEBP overexpression in osteoblastic cells.

• Journal of Animal Science and Technology
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• v.56 no.8
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• pp.33.1-33.8
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• 2014

Background: Sox 9 is a major marker of chondrocyte differentiation. When chondrocytes are cultured in vitro they progressively de-differentiate and this is associated with a decline in Sox 9 expression. The active form of vitamin D, 1, 25 $(OH)_2D_3$ has been shown to be protective of cartilage in both humans and animals. In this study equine articular chondrocytes were grown in culture and the effects of 1, 25 $(OH)_2D_3$ upon Sox 9 expression examined. The expression of the transient receptor potential vanilloid (TRPV) ion channels 5 and 6 in equine chondrocytes in vitro, we have previously shown, is inversely correlated with de-differentiation. The expression of these channels in response to 1, 25 $(OH)_2D_3$ administration was therefore also examined. Results: The active form of vitamin D (1, 25 $(OH)_2D_3$ when administered to cultured equine chondrocytes at two different concentrations significantly increased the expression of Sox 9 at both. In contrast 1, 25 $(OH)_2D_3$ had no significant effect upon the expression of either TRPV 5 or 6 at either the protein or the mRNA level. Conclusions: The increased expression of Sox 9, in equine articular chondrocytes in vitro, in response to the active form of vitamin D suggests that this compound could be utilized to inhibit the progressive de-differentiation that is normally observed in these cells. It is also supportive of previous studies indicating that $1{\alpha}$, 25-dihydroxyvitamin $D_3$ can have a protective effect upon cartilage in animals in vivo. The previously observed correlation between the degree of differentiation and the expression levels of TRPV 5/6 had suggested that these ion channels may have a direct involvement in, or be modulated by, the differentiation process in vitro. The data in the present study do not support this.

• Journal of the Korean Dietetic Association
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• v.23 no.1
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• pp.39-53
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• 2017

Insufficient vitamin D intake is a major health problem around the world. Recently, many studies have suggested that vitamin D intake may influence insulin resistance. However, little is known about the association between vitamin D and diabetes mellitus. The aim of this study was to investigate the association between serum 25-hydroxy vitamin D (25(OH)D) levels and diabetes mellitus in Korean adults. This study was a cross-sectional analysis of 3,686 participants of the Korean National Health and Nutrition Examination Survey (KNHANES) 2013~2014 aged 19 years and higher. The results showed that the mean serum 25-hydroxy vitamin D (25(OH)D) level in Korean adults was 16.77 ng/mL, and 74.2% of them had an insufficient serum 25-hydroxy vitamin D (25(OH)D) level (below 20 ng/mL). In normal and pre-diabetic groups, the serum 25-hydroxy vitamin D (25(OH)D) level significantly increased with age (P<0.001), but there was no significant difference relative to age in the diabetic group. Low vitamin D levels (25-hydroxy vitamin D < 10 ng/mL) were associated with increased fasting blood glucose levels, compared with optimal vitamin D levels (25-hydroxy vitamin D > 30 ng/mL), after adjusting for variables that may affect fasting blood glucose, but this result was not significant. In conclusion, although no significant association was observed between diabetes prevalence and vitamin D levels in this study, further studies are needed because the effect of vitamin D on diabetes remains controversial. This nutrient plays a crucial role in the body, and levels are insufficient in the Korean population.

• Tuberculosis and Respiratory Diseases
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• v.77 no.2
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• pp.73-80
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• 2014

Background: Low levels of serum vitamin D is associated with several lung diseases. The production and activation of matrix metalloproteinases (MMPs) may play an important role in the pathogenesis of emphysema. The aim of the current study therefore is to investigate if vitamin D modulates the expression and activation of MMP-2 and MMP-9 in human lung fibroblasts (HFL-1) cells. Methods: HFL-1 cells were cast into three-dimensional collagen gels and stimulated with or without interleukin-$1{\beta}$ (IL-$1{\beta}$) in the presence or absence of 100 nM 25-hydroxyvitamin D (25(OH)D) or 1,25-dihydroxyvitamin D ($1,25(OH)_2D$) for 48 hours. Trypsin was then added into the culture medium in order to activate MMPs. To investigate the activity of MMP-2 and MMP-9, gelatin zymography was performed. The expression of the tissue inhibitor of metalloproteinase (TIMP-1, TIMP-2) was measured by enzyme-linked immunosorbent assay. Expression of MMP-9 mRNA and TIMP-1, TIMP-2 mRNA was quantified by real time reverse transcription polymerase chain reaction. Results: IL-$1{\beta}$ significantly stimulated MMP-9 production and mRNA expression. Trypsin converted latent MMP-2 and MMP-9 into their active forms of MMP-2 (66 kDa) and MMP-9 (82 kDa) within 24 hours. This conversion was significantly inhibited by 25(OH)D (100 nM) and $1,25(OH)_2D$ (100 nM). The expression of MMP-9 mRNA was also significantly inhibited by 25(OH)D and $1,25(OH)_2D$. Conclusion: Vitamin D, 25(OH)D, and $1,25(OH)_2D$ play a role in regulating human lung fibroblast functions in wound repair and tissue remodeling through not only inhibiting IL-$1{\beta}$ stimulated MMP-9 production and conversion to its active form but also inhibiting IL-$1{\beta}$ inhibition on TIMP-1 and TIMP-2 production.

• Clinical and Experimental Pediatrics
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• v.58 no.8
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• pp.283-287
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• 2015

Purpose: We assessed the relationships between iron and vitamin D statuses in breastfed infants and their mothers and evaluated the determinants of iron and vitamin D deficiencies in breastfed infants. Methods: Seventy breastfed infants aged 4-24 months and their mothers participated in this study from February 2012 to May 2013. Complete blood counts, total iron binding capacity, and levels of C-reactive protein, iron, ferritin, calcium, phosphate, alkaline phosphatase, and 25-hydroxyvitamin D (25(OH)D) in infants and their mothers were measured. Results: A history of maternal prepregnancy anemia was associated with lower ferritin and 25(OH)D levels in both infants and their mothers. The 25(OH)D level of infants correlated with maternal 25(OH) D levels. The independent risk factors for iron deficiency in breastfed infants were the duration of breastfeeding (odds ratio [OR], 6.54; 95% confidence interval [CI], 1.09-39.2; P=0.04) and infant body weight (OR, 2.65; 95% CI, 1.07-6.56; P=0.04). The determinants for vitamin D deficiency were the infant's age (OR, 0.15; 95% CI, 0.02-0.97; P=0.046) and maternal 25(OH)D level (OR, 0.74; 95% CI, 0.59-0.92; P=0.01). Conclusion: A maternal history of prepregnancy anemia requiring iron therapy was associated with lower current ferritin and 25(OH)D levels in both infants and their mothers. Therefore, physicians should monitor not only iron but also vitamin D levels in infants who are breastfed by mothers who had prepregnancy anemia.

• Nutrition Research and Practice
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• v.5 no.5
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• pp.464-470
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• 2011

Growing evidence suggests an elevated risk for colorectal neoplasia among individuals with low levels of vitamin D, the biological actions of which are mediated by the vitamin D receptor (VDR). To investigate the association among vitamin D status, VDR polymorphisms (FokI, and BsmI), and colorectal adenoma, we conducted a meta-analysis of nine studies of circulating levels of 25-hydroxyvitamin D (25(OH)D) and five studies of FokI or BsmI polymorphisms in relation to colorectal adenomas. Study-specific relative risks (RRs) and 95% confidence intervals (CIs) were pooled using a random-effects model. A total of 3398 coloreetal adenomas for 25(OH)D and 1754 colorectal adenomas for VDR were included in the meta-analysis. We identified a significant inverse association between colorectal adenoma (combined RR, 0.93; 95% CI, 0.87-0.98 per 10 ng/mL increase in 25(OH)D levels). When we examined FokI and BsmI polymorphisms in the meta-analysis, we found no association for either FokI (combined RR, 1.00; 95% CI, 0.95-1.06) or BsmI (combined RR, 0.99; 95% CI, 0.93-1.05) in the additive model. These data suggest an inverse association between circulating 25(OH)D levels and colorectal adenoma risk.

• Nutrition Research and Practice
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• v.6 no.2
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• pp.162-168
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• 2012

Vitamin D deficiency is a risk factor for metabolic syndromes. We examined whether vitamin D deficiency altered the prevalence of cardiovascular disease (CVD) in older Koreans. Cross-sectional analysis of data from the Korean National Health and Nutrition Examination Survey IV 2008-2009 was used to examine the association between serum 25-hydroxyvitamin D (25(OH)D) levels and the prevalence of CVD in a representative population-based sample of 5,559 men and women aged ${\geq}50$ years. CVD was defined as angina pectoris, myocardial infarction, or stroke. The prevalence of CVD (7.0%) in the older Korean population was lower than that in the older US population, although average serum 25(OH)D levels were much lower in the Korean population. Additionally, serum 25(OH)D levels did not differ significantly between the CVD and non-CVD groups. However, subjects in the lowest category (< 25 nmol/l) of serum 25(OH)D level had the greatest prevalence of CVD, about two-fold higher than subjects in the highest category (> 75 nmol/l), after adjusting for age, gender, body mass index, education level, residence location, and region. The prevalence of other risk factors for CVD, including higher waist circumference, fasting glucose, low-density lipoprotein (LDL) cholesterol, and triglyceride levels and lower high-density lipoprotein (HDL) cholesterol levels, was also higher among subjects in the lowest category than among those in the highest category. In conclusion, low serum 25(OH)D may be an independent risk factor for CVD in older Koreans.

• Journal of Korea Entertainment Industry Association
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• v.13 no.5
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• pp.139-143
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• 2019

The aim of this study was to assess the association of vitamin D and urine microalbumin/creatinine (uACR) and obesity. The study subjects were Korean adults 20 years or older (n = 4,948) who participated in the Korea National Health and Nutrition Examination Survey 2012. Analysis of covariance test adjusted for covariates were performed for uACR levels in relation to vitamin D status [vitamin D deficient, 25(OH)D < 10 ng/dL; vitamin D insufficient, 25(OH)D ≥ 10, < 20 ng/dL; vitamin D sufficient, 25(OH)D ≥ 20 ng/dL]. The key study results were as follows: First, in the populations without obesity (BMI < 25 kg/m²), uACR levels were decreased with the increasing of vitamin D status (p < 0.001) after adjusting for relevant variables. Second, in the populations with obesity (BMI ≥ 25 kg/m²), the association between uACR levels and vitamin D status was not significant (p = 0.659). In conclusion, urine microalbumin/creatinine levels were inversely associated with vitamin D status in Korean adults without obesity, but not in Korean adults with obesity.

• Clinical and Experimental Pediatrics
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• v.58 no.3
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• pp.96-101
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• 2015

Purpose: Atopic dermatitis (AD) is a chronic inflammatory relapsing skin disorder. Vitamin D plays a pivotal role in the development of AD, and interleukin (IL) 31 is known to be related to pruritus in AD. The aim of our study was to determine whether 25-hydroxyvitamin D (25(OH)D) levels are related to IL-31 levels or to the severity of AD. Methods: We enrolled 91 children with AD and 32 control subjects without history or symptoms of allergic diseases. Blood was drawn to evaluate complete blood cell count, total eosinophil count (TEC), and total IgE, specific IgE to common allergens, 25(OH)D, and IL-31 levels. Serum 25(OH)D and IL-31 levels were measured using high-performance liquid chromatography and enzyme-linked immunosorbent assay, respectively. The scoring atopic dermatitis (SCORAD) index was used to evaluate the severity of AD. Results: The mean 25(OH)D level was significantly lower in the AD group than in the control group; 25(OH)D decreased greatly in the moderate and severe AD groups compared with the mild AD group. Children with atopic sensitization showed significantly lower 25(OH)D levels than nonatopic children. However, serum IL-31 levels were not related to AD group, SCORAD index, or 25(OH)D levels. The SCORAD index was inversely correlated with serum 25(OH)D level and positively correlated with TECs and total IgE levels. Children with moderate and severe AD had significantly higher TECs than children with mild AD. Conclusion: Vitamin D is related to the severity of AD independently of IL-31.

• Nutrition Research and Practice
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• v.18 no.1
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• pp.1-18
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• 2024

BACKGROUND/OBJECTIVES: Endoplasmic reticulum (ER) stress in adipose tissue causes an inflammatory response and leads to metabolic diseases. However, the association between vitamin D and adipose ER stress remains poorly understood. In this study, we investigated whether 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) alleviates ER stress in adipocytes. MATERIALS/METHODS: 3T3-L1 cells were treated with different concentrations (i.e., 10-100 nM) of 1,25(OH)₂D₃ after or during differentiation (i.e., on day 0-7, 3-7, or 7). They were then incubated with thapsigargin (TG, 500 nM) for an additional 24 h to induce ER stress. Next, we measured the mRNA and protein levels of genes involved in unfold protein response (UPR) and adipogenesis using real-time polymerase chain reaction and western blotting and quantified the secreted protein levels of pro-inflammatory cytokines. Finally, the mRNA levels of UPR pathway genes were measured in adipocytes transfected with siRNA-targeting Vdr. RESULTS: Treatment with 1,25(OH)₂D₃ during various stages of adipocyte differentiation significantly inhibited ER stress induced by TG. In fully differentiated 3T3-L1 adipocytes, 1,25(OH)₂D₃ treatment suppressed mRNA levels of Ddit3, sXbp1, and Atf4 and decreased the secretion of monocyte chemoattractant protein-1, interleukin-6, and tumor necrosis factor-α. However, downregulation of the mRNA levels of Ddit3, sXbp1, and Atf4 following 1,25(OH)₂D₃ administration was not observed in Vdr-knockdown adipocytes. In addition, exposure of 3T3-L1 preadipocytes to 1,25(OH)₂D₃ inhibited transcription of Ddit3, sXbp1, Atf4, Bip, and Atf6 and reduced the p-alpha subunit of translation initiation factor 2 (eIF2α)/eIF2α and p-protein kinase RNA-like ER kinase (PERK)/PERK protein ratios. Furthermore, 1,25(OH)₂D₃ treatment before adipocyte differentiation reduced adipogenesis and the mRNA levels of adipogenic genes. CONCLUSIONS: Our data suggest that 1,25(OH)₂D₃ prevents TG-induced ER stress and inflammatory responses in mature adipocytes by downregulating UPR signaling via binding with Vdr. In addition, the inhibition of adipogenesis by vitamin D may contribute to the reduction of ER stress in adipocytes.