Maternal B12 Deficiency Predisposes Diabetes in Offspring

Vitamin B12 deficiency during pregnancy may predispose children to metabolic problems such as type-2 diabetes, according to a new study.

Researchers at the University of Warwick (Coventry, United Kingdom) and George Eliot Hospital (GEH; Nuneaton, United Kingdom) hypothesized that maternal B12 might program leptin levels in-utero, and therefore decided to investigate the potential association between maternal B12 and leptin in maternal adipose tissue, placental tissue, and cord blood. To do so, they paired 91 maternal venous and cord blood, 42 adipose tissue, and 83 placental tissue samples collected at delivery.

The results showed that B12 deficiency was common, at about 40% in mothers and 29% in neonates. Upon analysis, maternal B12 was independently associated with neonatal leptin, which was higher in adipose tissue and placental tissue from mothers with low B12. They concluded that maternal B12 deficiency adversely programs the leptin gene, changing levels at which the hormone is produced whilst the fetus grows. The study was presented at the Society for Endocrinology annual conference, held during November 2016 in Brighton (United Kingdom).

“The leptin can increase for two reasons; 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 lead author Adaikala Antonysunil, PhD, of the University of Warwick. “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.”

“The nutritional environment provided by the mother can permanently program the baby’s health,” added senior author Ponusammy Saravanan, PhD, of the University of Warwick and GEH. “We know that children born to under or over nourished mothers are at an increased risk of health problems such as type-2 diabetes, and 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.”

Leptin is a hormone made which regulates the amount of fat stored in the body by adjusting both the sensation of hunger and energy expenditures. Hunger is inhibited when the amount of fat stored reaches a certain level, causing satiety. Leptin is then secreted and circulates through the body, eventually activating leptin receptors in the arcuate nucleus. Energy expenditure is then increased both by the signal to the brain, and directly via leptin receptors on peripheral targets.

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University of Warwick
George Eliot Hospital