Chronic maternal inflammation or high-fat-feeding programs offspring obesity in a sex-dependent manner
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Chronic maternal inflammation or high-fat-feeding programs offspring obesity in a sex-dependent manner. / Dudele, A.; Hougaard, K. S.; Kjølby, M.; Hokland, M.; Winther, G.; Elfving, B.; Wegener, G.; Nielsen, A. L.; Larsen, A.; Nøhr, M. K.; Pedersen, S. B.; Wang, T.; Lund, S.
I: International Journal of Obesity, Bind 41, 2017, s. 1420-1426.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Chronic maternal inflammation or high-fat-feeding programs offspring obesity in a sex-dependent manner
AU - Dudele, A.
AU - Hougaard, K. S.
AU - Kjølby, M.
AU - Hokland, M.
AU - Winther, G.
AU - Elfving, B.
AU - Wegener, G.
AU - Nielsen, A. L.
AU - Larsen, A.
AU - Nøhr, M. K.
AU - Pedersen, S. B.
AU - Wang, T.
AU - Lund, S.
PY - 2017
Y1 - 2017
N2 - 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.
AB - 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.
U2 - 10.1038/ijo.2017.136
DO - 10.1038/ijo.2017.136
M3 - Journal article
C2 - 28588305
VL - 41
SP - 1420
EP - 1426
JO - International Journal of Obesity
JF - International Journal of Obesity
SN - 0307-0565
ER -
ID: 188196654