Association between minerals intake and childhood obesity: A cross-sectional study of the NHANES database in 2007-2014.

BACKGROUND: The roles of minerals in obesity received increasing attention recently due to its oxidant or antioxidant functions and effects on insulin and glucose metabolism that may be associated with obesity. Herein, this study aims to explore the association between minerals and obesity and body mass index (BMI) in children with different ages, and hope to provide some references for prevention and management in children with high-risk of obesity. METHODS: Data of children aged 2-17 years old were extracted from the National Health and Nutrition Examination Survey (NHANES) database in 2007-2014 in this cross-sectional study. Weighted univariate and multivariate logistic regression and liner regression analyses were used to screen covariates, and explore the association between minerals [including calcium (Ca), phosphorus (P), magnesium (Mg), iron (Fe), zinc (Zn), copper (Cu), sodium (Na), potassium (K) and selenium (Se)] and childhood obesity and BMI. The evaluation indexes were ß, odds ratios (ORs) and 95% confidence intervals (CIs). These relationships were also investigated in age subgroups. RESULTS: Among 10,450 eligible children, 1,988 (19.02%) had obesity. After adjusting for covariates, we found the highest quartile of dietary Fe [OR = 0.74, 95%CI: (0.58, 0.95)] and Zn [OR = 0.70, 95%CI: (0.54, 0.92)] intakes were associated with low odds of childhood obesity, while that of dietary Na intake seemed to be positively linked to childhood obesity [OR = 1.35, 95%CI: (1.05, 1.74)]. High dietary intakes of Ca, Na and K were positively associated with children's BMI, on the contrary, dietary Fe and Zn consumptions had a negative one (all P<0.05). Additionally, these associations were also found in children with different age (all P<0.05). CONCLUSION: Dietary Fe and Zn intakes played positive roles in reducing childhood obesity or BMI, while the intakes of Na should be controlled suitably.

SIRT3 improves alveolar epithelial cell damage caused by bronchopulmonary dysplasia through deacetylation of FOXO1.

BACKGROUND: Bronchopulmonary dysplasia (BPD) is a serious and long-term lung condition commonly observed in premature babies. Sirtuin 3 (SIRT3) has been reported to reduce pulmonary injury and pulmonary fibrosis. OBJECTIVE: The present study investigated the specific role of SIRT3 in BPD by establishing hyperoxia-induced BPD rat and cell models. Hematoxylin and eosin staining was used to observe pathological changes in lung tissues. MATERIALS AND METHODS: The expression levels of SIRT3 and forkhead box protein O1 (FOXO1), as well as its acetylation levels, were detected in hyperoxia-induced lung tissues and cells by Western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Levels of reactive oxygen species, superoxide dismutase, and malondialdehyde were assessed by using biochemical kits. Following SIRT3 overexpression, the levels of inflammatory cytokines were assessed by RT-qPCR. Apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nickend labeling (TUNEL) and Western blot analysis. Upon FOXO1 knockout, cell inflammation, oxidative stress and apoptosis were evaluated again. RESULTS: Compared to the control group, the SIRT3 and FOXO1 expression levels were decreased and the FOXO1 acetylation levels were increased in hyperoxia-induced lung tissues and cells. In addition, SIRT3 reduced hyperoxia-induced inflammation, oxidative stress, and apoptosis in A549 cells, and inhibited FOXO1 acetylation to activate FOXO1. However, FOXO1 knockdown reversed the effects of SIRT3 overexpression in hyperoxia-induced A549 cells. CONCLUSION: SIRT3 relieved alveolar epithelial cell damage caused by BPD via deacetylation of FOXO1, suggesting that SIRT3 could be a therapeutic target in BPD.

SIRT3 improves alveolar epithelial cell damage caused by bronchopulmonary dysplasia through deacetylation of FOXO1

Background: Bronchopulmonary dysplasia (BPD) is a serious and long-term lung condition commonly observed in premature babies. Sirtuin 3 (SIRT3) has been reported to reduce pulmonary injury and pulmonary fibrosis. Objective: The present study investigated the specific role of SIRT3 in BPD by establishing hyperoxia-induced BPD rat and cell models. Hematoxylin and eosin staining was used to observe pathological changes in lung tissues. Materials and methods: The expression levels of SIRT3 and forkhead box protein O1 (FOXO1), as well as its acetylation levels, were detected in hyperoxia-induced lung tissues and cells by Western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Levels of reactive oxygen species, superoxide dismutase, and malondialdehyde were assessed by using biochemical kits. Following SIRT3 overexpression, the levels of inflammatory cytokines were assessed by RT-qPCR. Apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nickend labeling (TUNEL) and Western blot analysis. Upon FOXO1 knockout, cell inflammation, oxidative stress and apoptosis were evaluated again. Results: Compared to the control group, the SIRT3 and FOXO1 expression levels were decreased and the FOXO1 acetylation levels were increased in hyperoxia-induced lung tissues and cells. In addition, SIRT3 reduced hyperoxia-induced inflammation, oxidative stress, and apoptosis in A549 cells, and inhibited FOXO1 acetylation to activate FOXO1. However, FOXO1 knockdown reversed the effects of SIRT3 overexpression in hyperoxia-induced A549 cells. Conclusion: SIRT3 relieved alveolar epithelial cell damage caused by BPD via deacetylation of FOXO1, suggesting that SIRT3 could be a therapeutic target in BPD (AU)

Association of screen exposure with psychosocial problems in primary school students.

Introduction: This study aimed to investigate the current status of screen exposure and the factors related to screen exposure in primary school students and explore the relationship between screen exposure and psychosocial problems, which may provide evidence for the scientific use of electronic products and psychological interventions used in these children. Methods: The parents of 811 primary school students aged 6-12 years received a questionnaire survey in Beijing between January 13 and January 16, 2022. The demographic data and daily screen exposure time were collected, and the Strengths and Difficulties Questionnaire (SDQ) about their children was administered online. Results: In 793 students, the average daily screen exposure of <2 h and ≥2 h was noted in 75.0% and 25% of patients, respectively. The mobile phone was the main medium for screen exposure (40.9%). The family's economic level, parental relationship, and main supervisor were related to screen exposure time (χ 2 = 44.8,14.5 and 12.4, P < 0.05). A low family economic level with a monthly income not meeting the basic living needs, poor parental relationship, and an elderly person responsible for supervision were related to increased screen exposure time. The abnormal emotional and behavioral symptoms, conduct problems, hyperactivity inattention, peer communication, prosocial behaviors, and a total difficulties score were found in 11.6%, 9.8%, 15.3%, 22.1%, 6.8%, and 13.4% of children, respectively. Excessive screen exposure was related to peer interaction and prosocial behaviors (χ 2 = 12.18 and 7.76, P < 0.05). The children with excessive screen exposure were more likely to have abnormal peer interaction (χ 2 = 12.09, P = 0.001) and prosocial behaviors (χ 2 = 7.76, P = 0.005). Excessive screen exposure was a risk factor for peer interaction problems (P < 0.05). Discussion: In conclusion, the detection rate of excessive screen exposure is higher in primary school students, which is related to the family's economic level, parental relationship, and main supervisor. Excessive screen exposure is harmful to the psychosocial health of these children, which is characterized by abnormal peer intercommunion and prosocial behaviors. More attention should be paid to screen exposure time in primary school students.