SFEBES2013 Poster Presentations Obesity, diabetes, metabolism and cardiovascular (67 abstracts)
Maternal B12 insufficiency predicts neonate's metabolic risk factors
Antonysunil Adaikalakoteswari 1 , Lawson Alexander 2 , Craig Webster 2 , Catherine Wood 3 , Neil Anderson 3 , Kavitha Sivakumar 1 , Philip McTernan 1 , Gyanendra Tripathi 1 , Manu Vatish 1 & Ponnusamy Saravanan 1,
1University of Warwick, Warwick, UK; 2Heartlands Hospital, Birmingham, UK; 3George Eliot Hospital, Nuneaton, UK.
Studies in India (vegetarian population) show that vitamin B12 insufficiency is common in pregnancy and independently predict adiposity and insulin resistance in the offspring. Epigenetic programming is postulated as, along with folic acid, B12 is crucial for DNA methylation. Therefore, we investigated whether maternal B12 levels in a non-vegetarian UK population predict metabolic risk of the offspring.
Paired maternal venous and cord blood samples (n=91) were collected at the time of elective caesarean section. Serum vitamin-B12 and folate were determined by electro-chemiluminescent immunoassay. Serum homocysteine was determined by liquid-chromatography with tandem-mass spectrometric detection (LC–MS/MS).
B12 insufficiency (<150 pmol/l) was common (mothers 40%; neonates 29%) but not folate insufficiency (<7 nmol/l) (11% only in mothers). Low B12 mothers had significantly higher BMI, triglycerides, cholesterol, LDL-cholesterol and homocysteine. The neonates of low B12 mothers had higher triglycerides, leptin, homocysteine and lower HDL-cholesterol. Correlation analysis showed that maternal B12 (r=0.648; P<0.001), folate (r=0.706; P<0.001) and homocysteine (r=0.756; P<0.001) are associated with the respective neonatal indices. Furthermore, maternal B12 was inversely associated with neonatal triglycerides, HOMA-IR, leptin, homocysteine and directly with HDL-cholesterol. In multiple regression analysis, adjusted for all likely confounders, maternal B12 independently predicted neonatal HDL-cholesterol (β=0.169; P=0.044; R2=8.6%), leptin (β=−0.662; P=0.002; R2=12.7%), homocysteine (β=−0.302; P=0.001; R2=14.7%) but not triglycerides or HOMA-IR.
Our study replicates the Indian observations in a non-vegetarian population that maternal B12 insufficiency predicts metabolic risk of the offspring, albeit in a selective group at delivery. Carefully designed studies with appropriate control group, looking at early pregnancy B12 are warranted to assess the causality of our observation. If replicated, this has the potential to reduce the burden of metabolic disorders in the offspring.
Declaration of funding: George Eliot NHS trust Diabetes research fund.
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Endocrine Abstracts
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