دراسة أعواز فيتامينات B9, B12, D كعوامل اختطار لآفات القلب الخلقية

الموضوعات

علوم بحتة وطبيعية

روابط وملفات

التعريف والنوع

رقم الوثيقة

0ed8c6c7-cb7d-436e-8a0a-0305c7aba307

رقم العقد

0

نوع الوسائط

Crawler

نوع المحتوى

الرسائل العلمية

صيغة المصدر

رسائل دكتوراة

نوع الملف

pdf text

أسماء الملفات

1958371_1.pdf

بيانات النشر

ترجمة العنوان

Study of Vitamins B9, B12, D Deficiencies as Risk Factors for Congenital Heart Lesions

ألقاب المؤلفين

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اللغة

Arabic

المصدر والدورية

اسم المصدر

دراسة أعواز فيتامينات B9, B12, D كعوامل اختطار لآفات القلب الخلقية

المحتوى والصفحات

عدد الصفحات

185

ترجمة الملخص

Introduction: Maternal nutrition is a causal factor for congenital defects(CHD), and congenital heart defects are the most prevalent (0.1% occurrence) in living births, in addition they cause abortion and still births (Tennstedt, Chaoui et al. 1999; Christianson, Howson et al. 2006). Among maternal nutritional factorsvitaminB9and vitamin B12 and related metabolic pathways -methionine cycle, choline-betaine-homocysteine pathway and transsulfuration pathway -have a very important role leading to nucleotides formation and methyl donation for different epigenetic processes and cellular energy regulation. In addition the vitamin D that is also related to epigenetics (Karlic and Varga 2011(, and the protein fetuin-A related to energy metabolism and insulin resistance (Dasgupta, Bhattacharya et al. 2010). Subjects and methods: The current study was designed as a case-control study, the case group included 112 patient affected with congenital heart defect –aged 1day to 3 years-and 80 of their mothers, the control group included 52 healthy age and sex matched child and 50 of their mothers. The following measurments were performed for each participant: folate (chemiluminescence immunoassay),S-adenosyl methionine SAM, S-adenosyl homocysteine SAH(UPLC-MS/MS method), methyl malonic Acid, homocysteine ,cystathionine (GCMS method) , holotranscobalamin (microparticle enzyme immunoassay) choline, betaine, dimethylglycine (UPLC-MS/MS), 25-hydroxy vitamin D, asymmetric dimethylarginine,(ADMA), fetuin-A, gluthatione (ELISA), complete blood count. Parameters levels were compared between cases and controls and their intercorrelations were studied. Results: Levels of folate, SAM, DMG, 25-OHDwere higher in CHD children compared to controls (p=0.009; p<0.001; p=0.007, p=0.008)respectively, and BET/DMG methylation index was lower 10.2 vs.7.5 p<0.001),we found higher levels of SAM in yonger children and this was associated with higher levels of cystathionine (p=0.003),MMA (p=0.002), betaine (p=0.018), choline (p<0.001), DMG (P<0.001).Multiple regression test for markers related to SAM levels selected CYS, MMA, and DMG as positive predictors, and age and HCY as negative predictors for this marker. And the elevation of MMA (vitamin B12 deficiency marker) above481 nmol/L was associated with the elevation of SAM, CYS, DMG and HCY. In regards of mothers, CHD mothers compared to control mothers had higher levels of DMG (p=0.010, and lower levels of BET/DMG (p=0.001) and SAH (p=0.028).The study of the correlations between maternalmarkers showed significant negative correlations between choline and both MMA (p=0.003) and homocysteine levels (p=0.046), while maternal cystathionine correlated directly to maternal DMG (p=0.019), and maternal SAM (p=0.011), finally maternal fetuin-A correlated negatively to maternal choline (p=0.011), DMG (p=0.049) and cystathionine (p=0.044), and also with DMG in their CHD children (p = 0.008).High SAM levels in CHD children was associated with high maternal DMG(p=0.031) and folate (p = 0.046).and there were negative correlations 183between 25-OHD in CHD children and their mothers SAH and ADMA levels. The odds ratio for low animal protein (red meat) consumption during pregnancy was 3.707.Conclusion: Our results showed a metabolic disturbance in the trans-and re-methylation process in children affected with congenital heart defects (CHD) and their mothers. This is presented by high levels of SAM and folate in CHD children, and low SAH in their mothers, with high DMG and low BET/DMG methylation ratio, in both CHD children and their mothers, which reflects a disturbance in folate and methionine metabolic pathways, that is partly related to vitamin B12 deficiency. The mentioned identical metabolic abnormality in CHD children and their mothers is mainly manifested by a metabolic need for the choline, betaine-homocysteine remethylation pathway (which was firstly revealed by our results as an important pathway in this group of patients). This study showed also an inability in effective transmethylation for both folate dependent and independent methylation pathways, this could be due to an attempt to conserve the methyl group or to an ineffective demethylation of SAM. This metabolic disturbance affect and is affected by the energy metabolism as the disturbed metabolites were correlated to fetuin-A, and it affects also vitamin D in CHD children, as their 25-OHD correlated to maternal methylation markers. Taken together, our results suggest a metabolic risk factor in mothers and their CHD affected fetus manifested by disturbed methyl group metabolism, and correlated to a specifiec metabolic environment, that is poor in essential amino acids, methionine and viamin B12 and that enhances choline and betaine consumption and fetuin-A secretion.

إشراف وإعداد

الإشراف

ريما عبيد, فايزة القبيلي

الإعداد

رنوه محمود السيد

الاقتباسات الببليوغرافية