scholarly journals Altered dietary ratio of folic acid and vitamin B12 during pregnancy influences the expression of imprinted H19/IGF2 locus in C57BL/6 mice

2021 ◽  
pp. 1-42
Author(s):  
Aatish Mahajan ◽  
Divika Sapehia ◽  
Beenish Rahat ◽  
Jyotdeep Kaur

Abstract Maternal folic acid and vitamin B12 (B12) status during pregnancy influence fetal growth. This study elucidated the effect of altered dietary ratio of folic acid and B12 on the regulation of H19/IGF2 locus in C57BL/6 mice. Female mice were fed diets with 9 combinations of folic acid and B12 for 4 weeks. They were mated and the offspring born (F1) were continued on the same diet for 6 weeks post-weaning and were allowed to mate. The placenta and fetal (F2) tissues were collected at day 20 of gestation. H19 overexpression observed under dietary deficiency of folate combined with normal B12 (BNFD) was associated with an increased expression of miR-675 in maternal and fetal tissues. Insulin-like growth factor 2 (IGF2), expression was decreased under folic acid deficient conditions combined with normal, deficient or over-supplemented state of B12 (BNFD, BDFD, BOFD) in fetal tissues along with B12 deficiency combined with normal folic acid (BDFN) in the placenta. The altered expression of imprinted genes under folic acid deficient conditions was related to decreased serum levels of folate and body weight (F1). Hypermethylation observed at the H19 differentially methylated region (DMR) (in BNFD) might be responsible for the decreased expression of IGF2 in female fetal tissues. IGF2 DMR2 was found to be hypomethylated and associated with low serum B12 levels with B12 deficiency in fetal tissues. Results suggest that the altered dietary ratio of folic acid and B12 affects the in-utero development of the fetus in association with altered epigenetic regulation of H19/IGF2 locus.

1966 ◽  
Vol 96 (3) ◽  
pp. 310-315 ◽  
Author(s):  
Fred Benjamin ◽  
Frank A. Bassen ◽  
Leo M. Meyer
Keyword(s):  

2021 ◽  
Vol 104 (2) ◽  
pp. 003685042110076
Author(s):  
Nazmi Mutlu Karakaş

Background: In this study, the aim was to evaluate the prevalence of vitamin D, vitamin B12, ferritin, and folate deficiencies in adolescence to clarify the need for early diagnosis and therapy. Methods: The medical records of adolescents between 10 and 18 years of age between 01 September 2018 and 28 February 2019 as healthy with non-specific complaints, or due to well-child care visits, were analyzed retrospectively. Results: A total of 1847/2507 (73.6%) adolescents were included in the study. The prevalence of vitamin D deficiency was 25.7% (n: 178/691). Vitamin B12 deficiency prevalence was 69.2% (n: 753/1088). The prevalence of anemia and ferritin deficiency was 4.8% and 13.26%. The prevalence of folate deficiency was 37.9% (n: 413/1088). VDD prevalence was statistically significantly higher in females than males (F/M:116/62). VB12D prevalence, the number and mean age of females with hemoglobin deficiency, and low ferritin levels was found to be statistically significantly higher in females than males. Conclusions: The prevalence of vitamin D, vitamin B12, folate deficiency and low ferritin levels was found to be high among adolescents. In particular, adolescents admitting with non-specific complaints and for control purposes in big cities must be considered to be at risk for the deficiency of these vitamins and low level of ferritin.


2016 ◽  
Vol 7 (3) ◽  
pp. 276-279 ◽  
Author(s):  
Gaytri Khatri ◽  
Vikram K Mahajan ◽  
Karaninder S Mehta ◽  
Krishan K Sharma ◽  
Satya Bhushan ◽  
...  

2013 ◽  
Vol 7 (4) ◽  
pp. 83 ◽  
Author(s):  
Suheyl Asma ◽  
Cigdem Gereklioglu ◽  
Ahmet Erdogan ◽  
Mahmut Yeral ◽  
Mutlu Kasar ◽  
...  

Blood ◽  
1965 ◽  
Vol 26 (3) ◽  
pp. 354-359 ◽  
Author(s):  
K. N. JEEJEEBHOY ◽  
S. M. PATHARE ◽  
J. M. NORONHA

Abstract Vitamin B12 deficiency was associated with a rise in unconjugated folates and marked depletion of intracellular conjugated folates. The changes could be reversed by giving vitamin B12. These results probably indicate a way by which vitamin B12 and folic acid are interrelated at the cellular level.


1995 ◽  
Vol 154 (10) ◽  
pp. 866-866 ◽  
Author(s):  
Pietro Strisciuglio ◽  
Daniela Concolino ◽  
Maria Teresa Moricca ◽  
Loris Rivalta ◽  
Giuseppe Parlato

1974 ◽  
Vol 47 (6) ◽  
pp. 617-630
Author(s):  
A. Lavoie ◽  
E. Tripp ◽  
A. V. Hoffbrand

1. The uptake of 14C from [methyl-14C]methyItetrahydrofolate was significantly reduced in the phytohaemagglutinin (PHA)-stimulated lymphocytes from nine patients with untreated pernicious anaemia compared with the uptake in seven normal subjects. 2. The uptake of 14C from [14C]methyltetrahydrofolate by the lymphocytes from seven of the patients with pernicious anaemia was consistently increased by addition of vitamin B12in vitro. 3. The proportion of 14C taken up from [14C]methyltetrahydrofolate transferred to non-folate compounds was found to be significantly reduced in the PHA-stimulated lymphocytes from nine patients with untreated pernicious anaemia compared with the proportion transferred in the PHA-stimulated lymphocytes from seven normal subjects. Addition of vitamin B12in vitro consistently increased the transfer in vitamin B12-deficient cells but had no consistent effect in normal cells. 4. Normal and vitamin B12-deficient PHA-stimulated lymphocytes took up [3H]folic acid and after 72 h incubation converted this largely into pteroylpolyglutamate forms. 5. The proportion of labelled lymphocyte folate as pteroylpolyglutamate after incubation with [3H]folic acid was the same in vitamin B12-deficient as in normal lymphocytes and the proportion of pteroylpolyglutamates formed in vitamin B12-deficient lymphocytes was unaffected by addition of vitamin B12in vitro. 6. No radioactivity could be decteted in pteroylpolyglutamates after incubating normal PHA-stimulated lymphocytes with [14C]methyltetrahydrofolate for 72 h, suggesting that pteroylpolyglutamate forms of folate cannot be made directly from methyltetrahydrofolate. 7. These results are consistent with the ‘methyltetrahydrofolate trap’ hypothesis in vitamin B12 deficiency. It is suggested that reduced synthesis of pteroylpolyglutamates reported by others in vitamin B12-deficient cells may be secondary to the failure of removal of the methyl group from methyltetrahydrofolate rather than to a direct effect of vitamin B12 deficiency on the enzyme responsible for pteroylpolyglutamate synthesis. 8. Reduced entry of methyltetrahydrofolate into vitamin B12-deficient cells may be secondary to failure of conversion of this compound into tetrahydrofolate.


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