Circulating levels of the cytokines IL10, IFNγ and resistin in an obese mouse model of developmental programming

M A Kępczyńska1, E T Wargent1, M A Cawthorne1

  • 1Clore Laboratory, University of Buckingham, Buckingham, UK.

Insights

Maternal high-fat diet during pregnancy alters key metabolic factors in the mother, potentially programming offspring for metabolic disease. Understanding these maternal changes is crucial for developing interventions to prevent future health issues in children.

Area of Science:

  • Reproductive biology
  • Metabolic disease research
  • Developmental programming

Background:

  • Early life environment significantly influences offspring's metabolic health.
  • Maternal obesity and diet are linked to increased offspring susceptibility to metabolic disorders.
  • Identifying specific maternal factors mediating these effects is critical for clinical interventions.

Purpose of the Study:

  • To investigate which maternal metabolic factors, altered by a high-fat diet, induce adverse metabolic programming in offspring.
  • To use a diet-induced obese mouse model to identify these mediating factors.

Main Methods:

  • Female C57Bl/6 mice were fed either a control chow or a high-fat diet for 10 weeks pre-mating and throughout gestation.
  • Maternal body weight, composition, glucose tolerance, and plasma levels of insulin, adiponectin, RBP4, leptin, resistin, and inflammatory cytokines were measured at gestational day 18.

Main Results:

  • High-fat-fed dams exhibited increased body weight, fat mass, fasting blood glucose, and plasma insulin compared to control dams.
  • Obese dams showed reduced plasma adiponectin and resistin but increased levels of inflammatory cytokines (IL6, IL10, IFNγ).
  • Pregnancy high-fat feeding alters maternal plasma adipokines and adipocytokines.

Conclusions:

  • Maternal high-fat diet during pregnancy induces significant metabolic and inflammatory changes in the dam.
  • These altered maternal factors may directly impact fetal development, potentially leading to metabolic programming.
  • Further research is needed to confirm the direct transfer and impact of these factors on fetal programming.

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