Long-term Consequences of Methyl Donor Deficiency during in Utero and Early Life Development on Markers of the Metabolic Syndrome
- Corresponding Author:
- Vânia D’Almeida
Department of Psychobiology
Universidade Federal de São Paulo
Rua Napoleão de Barros, 925, São Paulo, SP, Brazil
E-mail: [email protected]
Received Date: August 17, 2016; Accepted Date: September 12, 2016; Published Date: September 16, 2016
Citation: Cavalcante-Silva V, Fernandes L, Haseyama EJ, Agamme ALDA, Muniz MTC (2016) Long-term Consequences of Methyl Donor Deficiency during in Utero and Early Life Development on Markers of the Metabolic Syndrome. J Nutr Food Sci 6:555. doi: 10.4172/2155-9600.1000555
Copyright: © 2016 Cavalcante-Silva V, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The aim of the present study was to assess the consequences of maternal vitamin B deficiency in mice during early development on the offspring's biochemical and biometric parameters. Female mice received vitamin deficient or standard control diets for one month prior to pregnancy, during pregnancy and lactation. Their offspring were then divided into three groups: Control “CT” (offspring of control, breastfed by control mothers), deficient pregnancy “DP” (offspring of deficient mothers, breastfed by control mothers) and deficient pregnancy and lactation “DPL” (offspring of deficient mothers, breastfed by deficient mothers). The body, perigonadal white adipose tissue (PWAT), pericardial white adipose tissue (PCWAT), liver, kidney, spleen, heart and brain were weighed, and blood glucose, total cholesterol and triglycerides evaluated in female and male offspring at postnatal day (PND) 0, 28, 90 and 210. The results indicated that the dams exposure to vitamin B2, B9, B12 and choline deficiencies contributed to increased events related to cannibalization and/or dead pups observed at PND 1 (p<0.049) and decreased the body weight at birth of female (p<0.001) and male (p<0.02) offspring. The body weight of both DPL female (p<0.006) and male (p<0.01) offspring remained lower at PND 28. At PND 210 no statistically significant differences were observed in female (p>0.8) and male (p>0.09) offspring body weight, however a decrease in PWAT of DPL males was observed. The early exposure to methyl donor deficiency was not associated with increased body weight or changes in glucose, triglycerides and cholesterol metabolism, typical markers of the metabolic syndrome.