Maternal HFD promoted a proinflammatory microbiota and metabolic pathway profile at both ages, amplifying the weaning reaction (high visceral fat glucose uptake, IL6, liver CT density) and causing adult dysmetabolism (high post-systemic gut and liver glucose uptake in relation to hyperglycemia, with visceral fat being unable to compensate), and monocyte-macrophage dysfunction (low MCP1), increasing proneness for liver injury. This evidence concerns the gene IL6 and Hyperglycemia.