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

by Lu Wang, Wei Liu, Sitong Bi, Li Zhou, Lihua Li

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 β, 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 PP Conclusion

Dietary Fe and Zn intakes played positive roles in reducing childhood obesity or BMI, while the intakes of Na should be controlled suitably.

Notoginsenoside R1 attenuates brain injury in rats with traumatic brain injury: Possible mediation of apoptosis via ERK1/2 signaling pathway

by Xiaoxian Pei, Ling Zhang, Dan Liu, Yajuan Wu, Xiaowei Li, Ying Cao, Xiangdong Du

Traumatic brain injury (TBI) occurs worldwide and is associated with high mortality and disability rate. Apoptosis induced by TBI is one of the important causes of secondary injury after TBI. Notoginsenoside R1 (NGR1) is the main phytoestrogen extracted from Panax notoginseng. Many studies have shown that NGR1 has potent neuroprotective, anti-inflammatory, and anti-apoptotic properties and is effective in ischemia-reperfusion injury. Therefore, we investigated the potential neuroprotective effects of NGR1 after TBI and explored its molecular mechanism of action. A rat model of TBI was established using the controlled cortical impact (CCI) method. The expression levels of Bcl-2, Bax, caspase 3, and ERK1/2-related molecules in the downstream pathway were also detected by western blotting. The expression levels of pro-inflammatory cytokines were detected by real-time quantitative PCR. Nissl staining was used to clarify the morphological changes around the injury foci in rats after TBI. Fluoro-Jade B (FJB) and terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) fluorescence staining were used to detect the apoptosis of neural cells in each group of rats. The results showed that NGR1 administration reduced neurological deficits after TBI, as well as brain edema and brain tissue apoptosis. It also significantly inhibited the expression of pro-inflammatory cytokines. Furthermore, NGR1 decreased the expression levels of extracellular signal-regulated kinase (ERK) and p-RSK1, which are phosphorylated after trauma. This study suggests that NGR1 can improve neuronal apoptosis in brain injury by inhibiting the ERK signaling pathway. NGR1 is a potential novel neuroprotective agent for the treatment of secondary brain injury after TBI.