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Background: Childhood obesity is a worldwide critical health concern. We aimed to clarify whether eating behaviours increased the risk of childhood obesity. Methods: We recruited 2,049 pre-school children aged 3-6 years between 1 December 2021 and 31 January 2022 in Taizhou, China. Children's weight status was classified according to the International Obesity Task Force criteria, and their eating behaviours were evaluated using the Children's Eating Behaviour Questionnaire. Correlation analyses, linear regressions, and one-way ANCOVA. were performed to analyse the association between children's eating behaviours and weight status. Results: In 'Food Avoidant' subscales, the scores of satiety responsiveness (P < 0.001) and slowness in eating (P = 0.001) were negatively associated with body mass index z score among pre-school children of both sexes. In 'Food Approach' subscales, the score of enjoyment of food was positively associated with body mass index z score in both boys (P = 0.007) and girls (P = 0.035), but the association of scores of food responsiveness with body mass index z score was found only in girls (P = 0.001). Conclusion: Our results supported that pre-school children with low scores in 'Food Avoidant' subscales and high scores in 'Food Approach' scales were more likely to become obese.
RESUMO
OBJECTIVE: To investigate the effect of adenosine A2A receptor knockout (A(2A)RKO) on relationship between continuous activation of phospho-c-Jun N-terminal kinase (P-JNK) and expression of nerve cell apoptosis in hippocampus CA1 domain of newborn mice after hypoxia/ischemia brain damage(HIBD) and its potential mechanism. METHODS: A(2A)RKO mice and adenosine A2A receptor wildtype (A(2A)RWT) littermates (n = 80) were divided into Sham operation group (S) and model group (M), 1, 3 and 7 day after HIBD, totally 8 groups. HIBD was developed with 7 day-old neonatal mice according classical Rice-Vannucci method. It was tested the effect of A(2A)RKO on short-term neurofunctional outcomes consisted of three developmental reflexes (righting, geotaxis and cliff aversion), the changes of brain pathology with hematoxylin-eosin (HE) staining and Nissl staining, the expressions of nerve cell apoptosis with terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling(TUNEL) staining and P-JNK were observed by immunohistochemistry. RESULTS: The neurological behavior injuries and brain histopathological damages and nerve apoptosis cells were aggravated in A(2A)RKO newborn mice after HIBD. The positive expressions of P-JNK were significantly higher in the ischemic hippocampus CA1 domain after HIBD than ones in group S respectively (P < 0.01), reaching to peak at 1 day and then began gradually decreasing. P-JNK expression in model knockout(MKO) at 1, 3 and 7 day increased greatly compared to those in the previous time point of corresponding model wildtype (MWT) (P < 0.01, P < 0.05, P > 0.05); there was a positive correlation between the expressions of P-JNK and nerve cell apoptosis after HIBD in newborn mice(r = 0.837, P < 0.01). CONCLUSION: Early continuous activation of P-JNK might be involved in the aggravated nerve apoptosis cells and brain damage induced by A(2A) RKO newborn mice after HIBD.
