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B12 deficiency can increase risk for type 2 diabetes

B12 deficiency during pregnancy may predispose baby into adulthood for metabolic problems such as type-2 diabetes.


Research presented at the Society for Endocrinology annual Conference in Brighton, United Kingdom still needs peer review testing to validate findings, however, could lead to a review of current vitamin B12 requirements for pregnant women through improved diet or supplements.


National Institutes of Health suggests daily B12

• teens over 14 years 2.4 mcg
• pregnant women 2.6 mcg
• lactating women 2.8 mcg

*mcg = micrograms
Please ask a medical professional how to interpret these amounts for your own daily intake.


Vitamin B12 is naturally found in animal products, including fish, meat, poultry, eggs and milk. This means that deficiency is more likely in those following a vegan diet. Previous studies show that mothers with low B12 levels had a higher BMI and were more likely to give birth to babies with low birth weight as well as high cholesterol levels. These children also had higher insulin resistance in childhood - a risk factor for type-2 diabetes.


Researchers at the University of Warwick Medical School speculate changes due to B12 deficiency may result in abnormal levels of leptin - the hormone which makes us feel full after eating.


Leptin is produced by fat cells and its level rises in response to eating. While lean diets are associated with normal leptin levels, obesity causes leptin to remain consistently higher than normal.

Higher leptin can eventually lead to leptin resistance, which drives overeating and increased risk for insulin resistance — or type-2 diabetes.


Babies born to mothers with B12 deficiency had higher than normal leptin levels.

This suggests mom's B12 deficiency can reprogram the fetal leptin gene.


"The nutritional environment provided by the mother can permanently program her baby's health," said Dr Ponusammy Saravanan, senior author of the study. "We know that children born to under or over nourished mothers are at an increased risk of health problems such as type-2 diabetes. We also see that maternal B12 deficiency may affect fat metabolism and contribute to this risk. This is why we decided to investigate leptin, the fat cell hormone."

The next steps in the study will be to determine the details of how and why the leptin increase is seen in babies born to mothers with low B12.


"Leptin can increase for two reasons:
[1] Either low B12 drives fat accumulation in the fetus, and this leads to increased leptin, or
[2] low B12 actually causes chemical changes in placental genes that produce leptin — making more of the hormone.

"As B12 is involved in methylation reactions in the body — which can affect whether genes are turned on and off — we suspect it may be the latter."


Adaikala Antonysunil PhD, Warwick Medical School, University of Warwick, Coventry, United Kingdom, worked on the study.


Background: Evidences show that maternal vitaminB12 deficiency at periods of development influence metabolic status and degree of metabolic syndrome of the offspring into adulthood. VitaminB12 is required for the synthesis of methionine, which is the precursor of S-adenosyl-methionine, a key methyl donor for DNA methylation. So vitaminB12 deficiency might cause methylation changes, which are thought to alter gene expression of regulatory factors and could result in adverse metabolic phenotypes. Our recent study showed that low maternal vitaminB12 was associated with adverse cord blood lipid profile and higher BMI which provided the clue to explore the link between the adiposity marker, leptin, and vitaminB12. We hypothesize that maternal B12 might program leptin levels in-utero. Therefore we investigated whether maternal B12 levels associate with leptin in maternal adipose tissue, placental tissue and cord blood.

Methods: Paired maternal venous and cord blood samples (n=91), adipose tissue (n=42) and placental tissue (n=83) were collected at delivery. Serum vitaminB12 was determined by electro-chemiluminescent immunoassay. Leptin levels were measured by ELISA. To assess the underlying mechanism, human pre-adipocyte cell line (Chub-S7) was differentiated in various B12 concentrations (1) Control: (B12-500 nM); (2) LowB12 (0.15 nM) (3) Control + methylation inhibitor (AZ): (B12-500 nM +5-Aza-dC-200 nM).

Results: B12 deficiency (<150 pmol/l) was common (mothers-40%; neonates-29%). In regression analysis, adjusted for likely confounders, maternal B12 independently associated with neonatal leptin (β=−0.662; P=0.002; R2=12.7%). Leptin gene expression was higher in adipose tissue and placental tissue from mothers with low B12. Leptin gene was higher in adipocytes (Chubs-S7) cultured with low B12 (0.15 nM) and treated with normal B12 (500 nM) in the presence of methylation inhibitor (5-Aza-dC).

Conclusion: Our study highlights that low maternal B12 associates with higher leptin in cord blood, maternal adipose tissue and placental tissue, suggesting leptin gene could represent a mechanism of adverse programming either in the placental tissue or maternal adipose tissue.

The research was presented as a conference abstract showing only preliminary results, and has not been peer reviewed.

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Nov 16, 2016   Fetal Timeline   Maternal Timeline   News   News Archive   

Potential results in bitamin B12 misregulation. Maternal obesity causes leptin to rise and remain
consistently higher than normal. Higher leptin can eventually lead to leptin resistance,
continued overeating, and increased risk for insulin resistance — or type-2 diabetes.


 


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