z-logo
Premium
A maternal low protein diet programs glucose and fatty acid metabolism differentially in adult male and female mouse offspring
Author(s) -
Plosch Torsten,
Straten Esther M.E.,
Dijk Theo H.,
Bloks Vincent W.,
Verkade Henkjan J.,
Kuipers Folkert
Publication year - 2011
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.25.1_supplement.990.3
Subject(s) - offspring , endocrinology , medicine , biology , gestation , carbohydrate metabolism , pregnancy , metabolism , low protein diet , lipid metabolism , fatty acid metabolism , insulin resistance , metabolic syndrome , insulin , diabetes mellitus , genetics
Nutritional conditions during fetal life can influence the risk to develop the metabolic syndrome in adult life (‘metabolic programming’). We aimed to establish a mouse model of metabolic programming focusing on the effects of a maternal low protein diet during gestation on glucose and lipid metabolism in the adult offspring. Pregnant C57BL/6J mice received a control or a low protein diet throughout gestation. Offspring received a low fat diet or a high fat diet from 6–22 weeks of age. Glucose metabolism was studied with a whole‐body‐glucose test using [6,6‐ 2 H]‐glucose. Hepatic gene expression was characterized by microarray. Maternal low‐protein‐diet did not affect glucose metabolism in male offspring. Female offspring from normal‐protein fed dams was relatively resistant to diet‐induced metabolic dysregulation. Maternal low‐protein‐diet during gestation led to deteriorated insulin sensitivity upon high‐fat feeding in female offspring. Microarray analyses showed a sex‐specific effect of the maternal diet. We conclude that, in mice, maternal protein restriction during gestation does not change the glucose response to a high fat diet in male offspring. However, it changes fatty acid and glucose metabolism in female offspring in such a way that it resembles male metabolism. Supported by the Netherlands Heart Foundation, grant 2004T048.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here