New research has found that antenatal B12 deficiency may be tied to higher than normal leptin levels in offspring, which can lead to type 2 diabetes.

Leptin is the hormone that informs the body that it is full after eating. Levels rise in response to eating while obesity causes levels to remain higher than normal. This can eventually lead to leptin resistance, continued overeating, and an increased risk of insulin resistance, which leads to type 2 diabetes. 

The study was conducted by researchers from the University of Warwick who collected maternal venous and cord blood samples (n=91), adipose tissue (n=42) and placental tissue(n=83) at delivery. They measured serum vitamin B12 by electro-chemiluminescent immunoassay, and leptin levels were measured by ELISA.  

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A regression analysis, adjusted for confounders, found that maternal B12 was independently associated with neonatal leptin (P=0.002). Additionally, leptin had higher gene expression in adipose tissue and placental tissue from mothers with low B12. The findings suggest that maternal B12 deficiency can negatively program the leptin gene, altering the levels at which the hormone is produced while the fetus grows.

“Either low B12 drives fat accumulation in the fetus, and this leads to increased leptin, or the low B12 actually causes chemical changes in the placental genes that produce leptin, making more of the hormone,” said Dr. Adaikala Antonysunil, one of the researchers. “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.”

These findings are preliminary results which will be presented at the Society for Endocrinology BES 2016 Conference.

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