Initial evidence for hypothalamic gliosis in children with obesity by quantitative T2 MRI and implications for blood oxygen-level dependent response to glucose ingestion.
gliosis
hypothalamus
magnetic resonance imaging
obesity
Journal
Pediatric obesity
ISSN: 2047-6310
Titre abrégé: Pediatr Obes
Pays: England
ID NLM: 101572033
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
23
05
2018
revised:
16
09
2018
accepted:
30
09
2018
pubmed:
12
12
2018
medline:
4
6
2019
entrez:
12
12
2018
Statut:
ppublish
Résumé
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. 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. 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). 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.
Identifiants
pubmed: 30537237
doi: 10.1111/ijpo.12486
pmc: PMC7027952
mid: NIHMS1061323
doi:
Substances chimiques
Glucose
IY9XDZ35W2
Oxygen
S88TT14065
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e12486Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK098466
Pays : United States
Organisme : University of Washington Royalty Research Fund
Pays : International
Organisme : Trust in Science Initiative from Glaxo-SmithKline, UK
Pays : International
Organisme : Fundação de Amparo à Pesquisa do Estado de São Paulo
ID : 2009/50809-5
Pays : International
Organisme : NIDDK NIH HHS
ID : R01 DK089036
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK035816
Pays : United States
Organisme : NIH HHS
ID : R01DK089036 and R01DK098466
Pays : United States
Organisme : Conselho Nacional de Desenvolvimento Científico e Tecnológico
Pays : International
Organisme : University of Washington Nutrition and Obesity Research Center
ID : P30DK035816
Pays : International
Informations de copyright
© 2018 World Obesity Federation.
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