November 08, 2016
2 min read

Maternal B12 levels associated with leptin levels in placental tissue, cord blood

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Babies born to mothers deficient in vitamin B12 were more likely to have higher than normal leptin levels, according to study findings presented at the Society for Endocrinology Annual Conference.

“The nutritional environment provided by the mother can permanently program the baby’s health,” Ponnusamy Saravanan, MBBS, FRCP, PhD, associate clinical professor at the University of Warwick Medical School, said in a press release. “We know that children born to under or overnourished mothers are at an increased risk for health problems, such as type 2 diabetes, and we also see that maternal B12 deficiency may affect fat metabolism and contribute to this risk.”

Saravanan and colleagues analyzed data from paired maternal venous and cord blood samples (n = 91), adipose tissue (n = 42) and placental tissue (n = 83), all collected at time of delivery. Researchers assessed serum B12 levels by electrochemiluminescent immunoassay and leptin levels by enzyme-linked immunosorbent assay (ELISA).

To assess the underlying mechanism, researchers differentiated the human pre-adipocyte cell line (Chub-S7) in various B12 concentrations: control (B12, 500 nM); low B12 (0.15 nM) and control with methylation inhibitor (B12, 500 nM + 5-Aza-dC 200 nM).

Within the cohort, 40% of mothers and 29% of neonates were vitamin B12 deficient (concentrations of 150 pmol/L or less), according to researchers. In regression analysis, maternal B12 was independently associated with neonatal leptin (P = .002), and leptin gene expression was higher in adipose tissue and placental tissue from mothers with low B12 levels, according to researchers.

Leptin gene expression was also higher in adipocytes cultured with low B12 (0.15 nM) and treated with normal B12 (500 nM) in the presence of a methylation inhibitor (5-Aza-dC), the researchers noted.

Saravanan said the study must be replicated in a prospective cohort, looking at the objective adiposity measures of the offspring, and in a long-term cohort study on the risk for childhood obesity and other metabolic disorders.

“The study provides more evidence for the intergenerational transmission of metabolic risk to the offspring, and the importance of the first 1,000 days of life in reducing the burden of metabolic disorders in adult life,” Saravanan told Endocrine Today. “It requires replication, and if proven, it may provide opportunity to reduce the burden of metabolic disorders by providing an optimal nutritional environment during the intrauterine life.” – by Regina Schaffer


Adaikalakoteswari A, et al. Abstract #P188. Presented at: Society for Endocrinology Annual Conference; Nov. 7-9, 2016; Brighton, United Kingdom.

Disclosure: Saravanan reports no relevant financial disclosures.