Maternal B12 Deficiency May up Diabetes Risk in Babies
Women with vitamin B12 deficiency during pregnancy may predispose their children to metabolic diseases such as Type-2 diabetes, a team of researchers led by one of Indian origin has warned.
The vitamin is found in animal products, including fish, meat, poultry, eggs and milk.
Its deficiency are more likely to occur in pregnant women, who follow a vegetarian diet, the study said.
“The nutritional environment provided by the mother can permanently programme the baby’s health,” said Ponusammy Saravanan, Associate Clinical Professor at the University of Warwick in Britain.
In this study, researchers hypothesised that the changes associated with B12 deficiency may be the result of abnormal levels of leptin – the hormone that tells us we are full after eating.
“Maternal B12 deficiency may affect fat metabolism and contribute to this risk. This is why we decided to investigate leptin, the fat cell hormone,” Saravanan added.
Leptin is produced by human body’s fat cells and its levels rise in response to eating food.
While lean diets are associated with normal levels of leptin, obesity causes levels to rise and remain consistently 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 researchers observed, adding that leptin can provide an effective ‘marker’ for body fat.
The study showed that babies born to mothers with B12 deficiency had higher than normal leptin levels.
This suggests that maternal B12 deficiency can adversely programme the leptin gene, changing the levels at which the hormone is produced while the foetus grows.
“The leptin can increase for two reasons. Either low B12 drives fat accumulation in the foetus, 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,” explained Adaikala Antonysunil from University of Warwick.
The study was presented at the Society for Endocrinology’s annual Conference in Brighton.
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