Intrauterine growth restriction induces persistent adipose inflammation and metabolic abnormalities in rats among various postnatal growth trajectories.

Hk3 , which catalyzes the initial glucose phosphorylation step critical for multiple glucose metabolic pathways, demonstrated an increasing trend in 3-month-old R groups, with significant upregulation observed in adipose tissue of the 9-month-old RC group [ 34 ].

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The findings revealed that while catch-up growth was a crucial factor in the development of adipose and metabolic abnormalities in IUGR offspring, the impact of IUGR itself was also highly significant.

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