Enduring consequences of maternal obesity for brain inflammation and behavior of offspring

Area of Science:

• Neuroscience
• Immunology
• Developmental Biology

Background:

• Obesity is a systemic inflammatory condition linked to cognitive dysfunction.
• Maternal obesity may transfer peripheral inflammation to the developing offspring brain, affecting cognition.

Purpose of the Study:

• To investigate if maternal obesity-induced peripheral inflammation affects offspring brain, specifically the hippocampus.
• To determine if this inflammation leads to cognitive dysfunction in offspring.

Main Methods:

• Rat dams were fed high-saturated-fat (SFD), high-trans-fat (TFD), or low-fat (LFD) diets before and during pregnancy/lactation.
• Offspring body weight, hippocampal microglial activation, and peripheral/hippocampal cytokine expression (post-lipopolysaccharide challenge) were assessed.
• Anxiety-like behavior and spatial learning were evaluated in adult offspring.

Main Results:

• SFD/TFD diets increased body weight in dams and pups.
• SFD/TFD pups showed increased hippocampal microglial activation at birth.
• Adult SFD/TFD offspring exhibited heightened inflammation and impaired anxiety and spatial learning, even after weaning onto a standard diet.

Conclusions:

• Maternal obesity, via high-fat diet, programs offspring for heightened inflammation and cognitive deficits.
• Early-life exposure to maternal obesity-associated inflammation impacts brain function and behavior long-term.
• Hippocampal neuroinflammation and altered microglial activity are key mechanisms linking maternal obesity to offspring cognitive dysfunction.