Perinatal high-fat diet induces systemic inflammation via altered tight junction complex organization during development and decreases expression of intestinal satiety peptides in male offspring.

Male rat offspring exposed to maternal high-fat diet in gestation and lactation show reduced vagal innervation in the nucleus of the solitary tract and lower small-intestinal CCK, GLP-1, and PYY expression in adulthood.

• Why it matters: Maternal obesity is linked to higher offspring obesity and comorbidities, but mechanisms connecting early diet exposure to later gut-brain dysfunction and inflammation remain unclear.
• What they did: Rats were fed a high-fat diet during gestation and lactation; adult offspring had small-intestinal satiety hormone and C-fiber innervation measured, and at weaning inflammatory mediators and colonic microbial metabolites were assessed.
• The result: At weaning, high-fat offspring had higher CRP and IL-1{beta} and lower microbially produced colonic short-chain fatty acids, alongside reduced Claudin-1 and ZO-1 colocalization in males, implying impaired barrier-linked gut-brain development.

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