Originally, vitamin K was defined as a factor for blood coagulation. Now more attention is focused on vitamin K for bone metabolism and bone health. Vitamin K is a coenzyme for glutamate carboxylase which converts glutamate residues to ${\gamma}$-carboxyglutamate(Gla) residues. Gla residues have calcium binding ability and bound to hydroxyapatite crystals in bone. Vitamin K promotes the carboxylation of osteocalcin and matrix Gla-protein, vitamin K-dependent proteins and improves bone mineral density and bone mass. Vitamin K deficiency causes reductions in bone mineral density and increases the risk of osteoporotic bone fractures, resulting from undercarboxylated osteocalcin. This paper is to provide a brief information of vitamin K and its role in bone health.
Kim, Hye-Jin;Kim, Jin-Woo;Jang, Soong-Nang;Kim, Kyung Do;Yoo, Jun-Il;Ha, Yong-Chan
Journal of Bone Metabolism
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v.25
no.4
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pp.267-274
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2018
Background: This prospective cohort study used nationwide claims data to investigate the incidence of fall and fragility fractures in association with urinary incontinence (UI) in the elderly, and to compare mortality after fragility fractures in elderly patients with or without incontinence. Methods: A total of 39,854 Korean adults (age, 66-80 years) who participated in health examinations between 2007 and 2012 and were followed up until 2015 were analyzed. Patient and comparison groups were classified according to the presence or absence of UI. The cumulative incidence of osteoporotic fragility fractures and falls in the 2 groups was assessed and compared. Hazard ratios for fragility fractures were calculated for the risk of UI in association with falls using a Cox proportional hazards model. Results: Of 39,854 elderly participants, 5,703 were classified in the UI group, while 34,151 were placed in the comparison group. Fall rates were significantly higher (20.8%) in the incontinence group than in the comparison group (4.7%) (P<0.001). Women in the incontinence group (13.9%) showed a significantly higher incidence of all types of fragility fractures than those in the comparison group (11.8%) (P=0.005). After adjustment for confounders, UI was not a significant risk factor for fragility fractures in men (P=0.878) or women (P=0.324). Conclusions: This study demonstrated that elderly women with UI have a significantly higher incidence of osteoporotic fragility fractures. In addition, elderly women are at higher risk for falls.
Skeletal muscle, essential for metabolism, thermoregulation, and immunity, undergoes myogenic differentiation that results in myotube formation. Trans-anethole (TA), the major constituent in essential oil produced by anise, star anise, and fennel, whose function in skeletal muscle has not yet been elucidated. Therefore, we investigated whether TA influenced muscle differentiation in mouse C2C12 myoblasts. Cells were induced to differentiate using a differentiation medium with or without TA (50 or 200 mg/mL) daily for 5 days. We measured myotube length and diameter after differentiation days 1, 3, and 5 and analyzed the expression of myogenic markers (myoblast determination protein 1, myogenin, myocyte enhancer factor 2, muscle creatine kinase, and myosin heavy chain) and atrophy-related genes (atrogin-1 and muscle ring finger-1 [MuRF-1]) using quantitative real-time PCR. Additionally, we observed the expression of total protein kinase B (Akt) and phosphorylated Akt (p-Akt) using western blotting. Our data showed that TA significantly induced the formation of smaller and thinner myotubes and reduced the myogenic factor expression. Furthermore, the atrogin-1 and MuRF-1 expression markedly increased by TA. Consistent with these findings, TA significantly decreased the expression of total Akt and p-Akt. Taken together, these results indicate that TA inhibits myogenic differentiation of C2C12 cells via reduction of both total Akt and p-Akt. Our findings may provide valuable insights into the impact of PAA on individuals at risk of muscle atrophy.
BACKGROUND/OBJECTIVES: A high-fat diet (HFD) induces obesity, which is a major risk factor for cardiovascular disease and cancer, while a calorie-restricted diet can extend life span by reducing the risk of these diseases. It is known that health effects of diet are partially conveyed through epigenetic mechanism including DNA methylation. In this study, we investigated the genome-wide hepatic DNA methylation to identify the epigenetic effects of HFD-induced obesity. MATERIALS AND METHODS: Seven-week-old male C57BL/6 mice were fed control diet (CD), calorie-restricted control diet (CRCD), or HFD for 16 weeks (after one week of acclimation to the control diet). Food intake, body weight, and liver weight were measured. Hepatic triacylglycerol and cholesterol levels were determined using enzymatic colorimetric methods. Changes in genome-wide DNA methylation were determined by a DNA methylation microarray method combined with methylated DNA immunoprecipitation. The level of transcription of individual genes was measured by real-time PCR. RESULTS: The DNA methylation statuses of genes in biological networks related to lipid metabolism and hepatic steatosis were influenced by HFD-induced obesity. In HFD group, a proinflammatory Casp1 (Caspase 1) gene had hypomethylated CpG sites at the 1.5-kb upstream region of its transcription start site (TSS), and its mRNA level was higher compared with that in CD group. Additionally, an energy metabolism-associated gene Ndufb9 (NADH dehydrogenase 1 beta subcomplex 9) in HFD group had hypermethylated CpG sites at the 2.6-kb downstream region of its TSS, and its mRNA level was lower compared with that in CRCD group. CONCLUSIONS: HFD alters DNA methylation profiles in genes associated with liver lipid metabolism and hepatic steatosis. The methylation statuses of Casp1 and Ndufb9 were particularly influenced by the HFD. The expression of these genes in HFD differed significantly compared with CD and CRCD, respectively, suggesting that the expressions of Casp1 and Ndufb9 in liver were regulated by their methylation statuses.
Background: Genetic and environmental factors play important roles in pathogenesis of digestive tract cancers like those in the esophagus, stomach and colorectum. Folate deficiency and methylenetetrahydrofolate reductase (MTHFR) as an important enzyme of folate and methionine metabolism are considered crucial for DNA synthesis and methylation. MTHFR variants may cause genomic hypomethylation, which may lead to the development of cancer, and MTHFR gene polymorphisms (especially C677T and A1298C) are known to influence predispositions for cancer development. Several case control association studies of MTHFR C677T polymorphisms and colorectal cancer (CRC) have been reported in different populations with contrasting results, possibly reflecting inadequate statistical power. Aim: The present meta-analysis was conducted to investigate the association between the C677T polymorphism and the risk of colorectal cancer. Materials and Methods: A literature search of the PubMed, Google Scholar, Springer link and Elsevier databases was carried out for potential relevant articles. Pooled odds ratio (OR) with corresponding 95 % confidence interval (95 % CI) was calculated to assess the association of MTHFR C677T with the susceptibility to CRC. Cochran's Q statistic and the inconsistency index (I2) were used to check study heterogeneity. Egger's test and funnel plots were applied to assess publication bias. All statistical analyses were conducted by with MetaAnalyst and MIX version 1.7. Results: Thirty four case-control studies involving a total of 9,143 cases and 11,357 controls were retrieved according to the inclusion criteria. Overall, no significant association was found between the MTHFR C677T polymorphism and colorectal cancer in Asian populations (for T vs. C: OR=1.03; 95% CI= 0.92-1.5; p= 0.64; for TT vs CC: OR=0.88; 95%CI= 0.74-1.04; p= 0.04; for CT vs. CC: OR = 1.02; 95%CI= 0.93-1.12; p=0.59; for TT+ CT vs. CC: OR=1.07; 95%CI= 0.94-1.22; p=0.87). Conclusions: Evidence from the current meta-analysis indicated that the C677T polymorphism is not associated with CRC risk in Asian populations. Further investigations are needed to offer better insight into any role of this polymorphism in colorectal carcinogenesis.
Journal of the Korean Association of Oral and Maxillofacial Surgeons
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v.28
no.5
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pp.364-371
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2002
Many chemical compopunds are converted into reactive electrophilic metabolites by the oxidative(Phase I) enzymes, which are mainly cytochrome P-450 enzyme(CYPs). Phase II conjugating enzymes, such as glutathione S-transferase(GST), usually act as inactivation of enzymes. Genetic polymorphisms have been found to be associated with increased susceptibility to cancer of the lung, bladder, breast and colorectal. Many of the polymorphic genes of carcinogen metabolism show considerably different type of cancer among different ethnic groups as well as individuals within the same group. The aim of this study is (1) to establish the frequencies of genetic polymorphisms of GSTM1 and CYP1A1 in Korean oral squamous cell carcinoma(SCC), (2) to associate oral SCC with the risk of these genetic polymorphisms. The genetic polymorphisms of the GSTM1 and the CYP1A1 genes among 50 Korean oral SCC were analyzed using polymerase chain reaction(PCR). The results suggest that the homozygote and the mutant type of CYP1A1 MspI polymorphisms may be associated with genetic susceptibility to oral SCC in Korean. A combination of the GSTM1 null type with the homozygote(m1/m1), and the mutant(m2/m2) type of CYP1A1 MspI polymorphisms showed a relatively high risk of oral SCC in Korean. In the smoking group, the GSTM1 wild genotype may be the high risk factor of oral SCC in Korean. These data coincide with the hypothesis which states that different susceptibility to cancer of genetic polymorphisms exist among different ethnic group and different types of human cancer.
N-acetyltransferase 2 (NAT2) is a polymorphic enzyme that plays an important role in the metabolism of various potential carcinogens. In recent years, a number of studies have been carried out to investigate the relationship between the rs1799930 and rs1799931 polymorphism in NAT2 and cancer risk in multiple populations for different types of cancer. However, the results were not consistent. Therefore, we performed a meta-analysis to further explore the relationship between NAT2 polymorphism and the risk of cancer. A total of 21 studies involving 15, 450 subjects for rs1799930 and 13, 011 subjects for rs1799931 were included in this meta-analysis. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess strength of associations. We also evaluated the publication bias and performed a sensitivity analysis. Overall, our results showed an apparent significant association between the NAT2 rs1799930 polymorphism and cancer susceptibility in Asians (GA vs. GG: OR=1.22, 95% CI=1.03-1.45; dominant model: OR=1.22, 95% CI=1.03-1.43) and population-based controls (GA vs. GG: OR=1.10, 95% CI=1.01-1.19; dominant model: OR=1.09, 95% CI=1.01-1.18). In contrast, a significant association was observed between the NAT2 rs1799931 G>A polymorphism and decreased cancer susceptibility in overall meta-analysis (AA vs. GG: OR=0.55, 95% CI=0.33-0.93; GA vs. GG: OR=1.00, 95% CI=0.88-1.14; dominant model: OR=0.97, 95% CI=0.86-1.10; recessive model: OR=0.56, 95% CI=0.34-0.94) and the Asian group (AA vs. GG: OR=0.50, 95% CI=0.26-0.94; recessive model, OR=0.50, 95% CI=0.27-0.94). We found that the NAT2 rs1799930 may be a risk factor, while the NAT2 rs1799931 polymorphism is associated with a decreased risk of cancer and is likely a protective factor against cancer development.
Lee, Bora;Heo, You Jung;Lee, Young Ah;Lee, Jieun;Kim, Jae Hyun;Lee, Seong Yong;Shin, Choong Ho;Yang, Sei Won
Annals of Pediatric Endocrinology and Metabolism
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v.23
no.4
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pp.196-203
/
2018
Purpose: The hemoglobin glycation index (HGI) represents the degree of nonenzymatic glycation and has been positively associated with cardiometabolic risk factors (CMRFs) and cardiovascular disease in adults. This study aimed to investigate the association between HGI, components of metabolic syndrome (MS), and alanine aminotransferase (ALT) in a pediatric nondiabetic population. Methods: Data from 3,885 subjects aged 10-18 years from the Korea National Health and Nutrition Examination Survey (2011-2016) were included. HGI was defined as subtraction of predicted glycated hemoglobin ($HbA1_c$) from measured $HbA1_c$. Participants were divided into 3 groups according to HGI tertile. Components of MS (abdominal obesity, fasting glucose, triglycerides, high-density lipoprotein cholesterol, and blood pressure), and proportion of MS, CMRF clustering (${\geq}2$ of MS components), and elevated ALT were compared among the groups. Results: Body mass index (BMI) z-score, obesity, total cholesterol, ALT, abdominal obesity, elevated triglycerides, and CMRF clustering showed increasing HGI trends from lower-to-higher tertiles. Multiple logistic regression analysis showed the upper HGI tertile was associated with elevated triglycerides (odds ratio, 1.65; 95% confidence interval, 1.18-2.30). Multiple linear regression analysis showed HGI level was significantly associated with BMI z-score, $HbA1_c$, triglycerides, and ALT. When stratified by sex, age group, and BMI category, overweight/obese subjects showed linear HGI trends for presence of CMRF clustering and ALT elevation. Conclusion: HGI was associated with CMRFs in a Korean pediatric population. High HGI might be an independent risk factor for CMRF clustering and ALT elevation in overweight/obese youth. Further studies are required to establish the clinical relevance of HGI for cardiometabolic health in youth.
Journal of the Korea Academia-Industrial cooperation Society
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v.18
no.4
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pp.267-274
/
2017
This is a non-experimental and retrospective study aimed at determining the effects of long-term hospitalization on the body mass index (BMI) and lipid metabolism in long-term hospitalized patients. The study subjects included 120 patients aged 40-65 years who were hospitalized for >3 months in 2 long-term care hospitals in Gyeonggi-do, South Korea. In this study, the BMI and levels of total cholesterol, triglycerides (TG), high-density lipoprotein (HDL), and low density lipoprotein (LDL) at admission and 3 months after hospitalization were compared and analyzed, and the related changes over time were followed up. The general characteristics of the subjects were analyzed by using descriptive statistics and frequency analysis. In addition, logistic regression analysis was performed to determine the effects of the general characteristics on the BMI and Dyslipidemia. The changes in the BMI and blood lipid levels between admission and 3 months after hospitalization were analyzed using the paired t-test. The results showed that with regard to the changes in the blood lipid levels, the triglyceride levels significantly increased 3 months after hospitalization (p<.05). These findings imply that long-term hospitalization for care and rehabilitation after acute-phase treatment should be considered a potential high-risk factor for dyslipidemia, which could be prevented or alleviated by providing the patients with health education, including exercise and dietary education.
It has been established that hypercholesterolemia is a major risk factor for atherosclerosis. Recent data showed that the incidence of hypercholesterolemia increase in Korea. n-3 Fatty acids lower serum triglyceride profoundly but the effect on serum cholesterol is not clear. This study was performed to assess the effects of low and moderate supplementation of marine n-3 fatty fish on serum cholesterol in young healthy korean woman. Nineteen subjects were divided into two groups. Each group receive an experimental diet supplemented with either 100g (group I) or 200g mackeral(Scomber japonicus) fish(group II) for 1-week. The diet was designed to avoid in which the amount of n-6 fatty acids would be much greater than that of n-3 fatty acids. MUFA, SFA intakes were similar in the two diets. The ratio of n-6/n-3 fatty acids was 1 : 1.l for group I, 1 : 2.51 for group II. The average daily n-3 fatty acids consumption from fish was 3.87g/day (1.03g EPA, 2.84g DHA)for group I, 7.74g/day (2.06g EPA, 5.68g DHA) for group II. Blood samples were obtained 2 times before experimental diet, immediately after experimental diet for 1-week. After experimental diet for 1-week, the serum total-cholesterol levels decreased significantly (16.4$\pm$15.1mg/dl, p<0.01) in group II and lowered slightly (13.7$\pm$25.8mg/dl)in group I. There were no significant changes from baseline to the end of the study in serum HDL-cholesteol, LDL-cholesterol, HDL-C/T-C ratio, and LDC-C/HDL-C ratio. The results suggest that the moderate levels of marine n-3 fatty fish consumption could improve serum cholesterol in normal subjects, therefore in might be of value in the prevention of atherosclerosis. However the clinical usefulness of moderate n-3 fatty fish consumption of hypercholesterolemic subjects will require further study. Also further studies are required to elucidate the long-term effects of low n-3 fatty fish consumtion.
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