Maternal methionine supplementation in mice affects long-term body weight and locomotor activity of adult female offspring

Autor(es)

Cavalcante-Silva, Vanessa ; da Silva Vallim, Julia Ribeiro ; Fernandes, Leandro ; de Oliveira, Allan Chiaratti ; D'Almeida, Vania

• Tipo de documento: Artigo Científico
• Fonte: BRITISH JOURNAL OF NUTRITION; v. 127, n. 8, p. 10-pg., 2021-06-14.

Resumo

Methionine is a precursor of s-adenosylmethionine, the main donor of methyl radicals for methylation of DNA and other compounds. Previous studies have shown that reduced availability of methyl radicals during pregnancy/lactation decreased offspring perigonadal white adipose tissue (PWAT) and body weight. Therefore, we aimed to evaluate the effects of methionine supplementation during early development, a time of great ontogenic plasticity, by assessing the biometric, biochemical and behavioural parameters of the offspring of adult Swiss female mice supplemented with 1 % methionine in water 1 month before pregnancy, during pregnancy or pregnancy/lactation. After birth, the offspring were distributed into three groups: control (CT), methionine supplementation during pregnancy (SP) and methionine supplementation during pregnancy and lactation (SPL), and were followed until postnatal day (PND) 300. No changes were observed in offspring birth weight in both sexes. At PND 5, 28 and 90, no differences in body weight were found in females; however, at PND 300, SP and SPL females showed an increase in body weight when compared with the control group. This increase in body weight was accompanied by a total and relative increase in PWAT, and a decrease in locomotor activity in these groups. No differences in the body and organ weights were found in male offspring. In conclusion, the increased availability of methyl radicals during pregnancy and lactation impacted long-term body composition and locomotor activity in female offspring. (AU)

• Processo FAPESP: 10/00075-2 - Hiper-homocisteinemia materna e alterações epigenéticas na programação fetal de genes envolvidos na etiopatogênese da Doença de Alzheimer
• Beneficiário: Vânia D'Almeida
• Modalidade de apoio: Auxílio à Pesquisa - Regular