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Initial evidence for hypothalamic gliosis in children with obesity by quantitative T2 MRI and implications for blood oxygen‐level dependent response to glucose ingestion

2018; Wiley; Volume: 14; Issue: 2 Linguagem: Inglês

10.1111/ijpo.12486

2047-6310

Letícia E. Sewaybricker, Ellen A. Schur, Susan J. Melhorn, Brunno Machado de Campos, Mary K. Askren, Guilherme Nogueira, Mariana Porto Zambon, Maria Ângela R. G. M. Antônio, Fernando Cendes, Lı́cio A. Velloso, Gil Guerra‐Júnior,

Advanced Neuroimaging Techniques and Applications

Summary Objective In adults, hypothalamic gliosis has been documented using quantitative T2 neuroimaging, whereas functional magnetic resonance imaging (fMRI) has shown a defective hypothalamic response to nutrients. No studies have yet evaluated these hypothalamic abnormalities in children with obesity. Methods Children with obesity and lean controls underwent quantitative MRI measuring T2 relaxation time, along with continuous hypothalamic fMRI acquisition to evaluate early response to glucose ingestion. Results Children with obesity (N = 11) had longer T2 relaxation times, consistent with gliosis, in the mediobasal hypothalamus (MBH) compared to controls (N = 9; P = 0.004). Moreover, there was a highly significant group*region interaction ( P = 0.002), demonstrating that signs of gliosis were specific to MBH and not to reference regions. Longer T2 relaxation times correlated with measures of higher adiposity, including visceral fat percentage ( P = 0.01). Mean glucose‐induced hypothalamic blood oxygen‐level dependent signal change did not differ between groups ( P = 0.11). However, mean left MBH T2 relaxation time negatively correlated with glucose‐induced hypothalamic signal change ( P < 0.05). Conclusion Imaging signs of hypothalamic gliosis were present in children with obesity and positively associated with more severe adiposity. Children with the strongest evidence for gliosis showed the least activation after glucose ingestion. These initial findings suggest that the hypothalamus is both structurally and functionally affected in childhood obesity.