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Multi‐vitamin supplementation during pregnancy leads to greater weight gain, impaired glucose tolerance and insulin resistance in rat offspring
Author(s) -
Szeto Ignatius Man Yau,
Das Paul J.,
Taha Ameer Y.,
Anderson G. Harvey
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1314-a
Background Multi‐vitamin consumption during pregnancy has increased significantly in the past 30 years concurrent with the rising prevalence of obesity. An increase in vitamin intake during pregnancy can alter the level of gene methylation and expression in the offspring. The purpose of this study was to determine whether multi‐vitamin supplementation during pregnancy increases the risk of obesity and insulin resistance in rat offspring. Methods Two groups of pregnant Wistar rats (n=10/group) were fed the AIN‐93 diet containing either 1X (control) or 10X the recommended amount of the AIN‐93 multi‐vitamin mix (VM). Pups were weaned to either the control diet or an obesity‐inducing liquid diet (n=20/group/gender). Body weight was measured weekly from birth. An oral glucose tolerance test (OGTT, 5g/kg) was performed every 4 to 5 weeks post‐weaning. Insulin resistance was measured by multiplying fasting glucose and insulin at 12 weeks post‐weaning; and fat pad mass were weighed. Results Compared to the pups born from VMx1 dams, pups from VMx10 dams had no difference in BW at birth, but had 7% lower BW at weaning (p<0.02) and 10% greater weight gain at 18 weeks post‐weaning (p<0.01), independent of pup gender and diet. Pups from VMx10 dams had a 40% higher blood glucose response (iAUC) during the OGTT starting at 9 weeks post‐weaning (p<0.05). At 12 weeks post‐weaning, insulin resistance was 40% higher (p<0.05) and fat pad mass was 20% higher (p<0.05) in pups from VMx10 dams. Conclusions Multi‐vitamin supplementation of rats during pregnancy leads to greater weight gain and insulin resistance in the offspring. Supported by CIHR.

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