Chronic maternal inflammation or high-fat-feeding programs offspring obesity in a sex-dependent manner
Research output: Contribution to journal › Journal article › Research › peer-review
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.
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.
Original language | English |
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Journal | International Journal of Obesity |
Volume | 41 |
Pages (from-to) | 1420-1426 |
Number of pages | 7 |
ISSN | 0307-0565 |
DOIs | |
Publication status | Published - 2017 |
ID: 188196654