Neonatal high-dose riboflavin attenuates abdominal adiposity and binge eating associated with adipose metabolic remodeling in experimental cerebral palsy

Objectives Maternal immune activation induced by lipopolysaccharide (LPS) exposure is a critical factor in the pathogenesis of cerebral palsy (CP). This early inflammatory response predisposes the postnatal brain to hypoxic injury and metabolic dysregulation. Although hypoxic injury and metabolic dysregulation are well characterized individually, their interplay in CP and the potential role of metabolic modulators remain poorly understood.Methods We investigated the metabolic state of male Wistar rats in a CP model induced by gestational LPS (200 μg/kg) and postnatal anoxia at P0, and the effects of neonatal high-dose riboflavin (100 mg/kg, P1–P21).Results CP increased body weight (p < 0.05 to p < 0.01) and food intake (p < 0.05), whereas riboflavin reduced both parameters (p < 0.05 to p < 0.01). Moreover, CP also reduced kinetic energy (p < 0.05) and mean velocity (p < 0.05 to p < 0.01), whereas riboflavin partially restored motor performance by increasing mean velocity (p < 0.05). Riboflavin attenuated CP-associated abdominal adiposity and glucose resistance (p < 0.05), while CP caused reduced serum lipid (p < 0.01 to p < 0.001) and hypothalamic Pomc/Npy dysfunction (p < 0.05 to p < 0.01). Riboflavin upregulated Slc2a4 (GLUT-4), dysregulated in CP (p < 0.05), and Ppargc1a (PGC-1α) in white and brown adipose tissues (p < 0.01 to p < 0.001), without affecting the hypothalamus, soleus muscle, or liver.Discussion Collectively, these findings suggest that CP associated with maternal–fetal inflammation and postnatal anoxia leads to persistent systemic metabolic disturbances affecting abdominal adiposity and binge-eating behavior, which may be modulated by neonatal high-dose riboflavin through tissue-specific effects on adipose tissue. (p-value ranges reflect different pairwise comparisons among groups).