A Dudele1, K S Hougaard2, M Kjølby3, M Hokland4, G Winther5, B Elfving5, G Wegener5, A L Nielsen4, A Larsen4, M K Nøhr6,7, S B Pedersen6,7, T Wang1, S Lund8. 1. Department of Bioscience, Section for Zoophysiology, Aarhus University, Aarhus, Denmark. 2. Department of Public Health, Section for Occupational and Environmental Health, University of Copenhagen, Copenhagen, Denmark. 3. Department of Biomedicine, The Danish Research Institute of Translational Neuroscience, Nordic EMBL Partnership for Molecular Medicine and Danish Diabetes Academy, Aarhus University, Aarhus, Denmark. 4. Department of Biomedicine, Aarhus University, Aarhus, Denmark. 5. Department of Clinical Medicine, Translational Neuropsychiatry Unit, Aarhus University, Risskov, Denmark. 6. Department of Clinical Medicine, Aarhus University, Aarhus, Denmark. 7. Department of Endocrinology and Metabolism C, Aarhus University Hospital, Aarhus, Denmark. 8. Department of Endocrinology and Internal Medicine Medical Research Laboratory, Aarhus University Hospital, Aarhus, Denmark.
Abstract
BACKGROUND/ OBJECTIVES: The current world-wide obesity epidemic partially results from a vicious circle whereby maternal obesity during pregnancy predisposes the offspring for accelerated weight gain and development of metabolic syndrome. Here we investigate whether low-grade inflammation, characteristic of the obese state, provides a causal role for this disastrous fetal programming in mice. METHODS: We exposed pregnant and lactating C57BL/6JBom female mice to either high-fat diet (HFD), or continuous infusion of lipopolysaccharide (LPS), a potent trigger of innate immunity, and studied offspring phenotypes. RESULTS: Both maternal LPS or HFD treatments rendered the offspring hyperphagic and inept of coping with a HFD challenge during adulthood, increasing their adiposity and weight gain. The metabolic effects were more pronounced in female offspring, while exposed male offspring mounted a larger inflammatory response to HFD at adulthood. CONCLUSIONS: This supports our hypothesis and highlights the programming potential of inflammation in obese pregnancies.
BACKGROUND/ OBJECTIVES: The current world-wide obesity epidemic partially results from a vicious circle whereby maternal obesity during pregnancy predisposes the offspring for accelerated weight gain and development of metabolic syndrome. Here we investigate whether low-grade inflammation, characteristic of the obese state, provides a causal role for this disastrous fetal programming in mice. METHODS: We exposed pregnant and lactating C57BL/6JBom female mice to either high-fat diet (HFD), or continuous infusion of lipopolysaccharide (LPS), a potent trigger of innate immunity, and studied offspring phenotypes. RESULTS: Both maternal LPS or HFD treatments rendered the offspring hyperphagic and inept of coping with a HFD challenge during adulthood, increasing their adiposity and weight gain. The metabolic effects were more pronounced in female offspring, while exposed male offspring mounted a larger inflammatory response to HFD at adulthood. CONCLUSIONS: This supports our hypothesis and highlights the programming potential of inflammation in obese pregnancies.
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