Erratum: Whole-transcriptome analysis of aluminum-exposed rat hippocampus and identification of ceRNA networks to investigate neurotoxicity of Al.

[This corrects the article DOI: 10.1016/j.omtn.2021.11.010.].

Chinese Healthy Eating Index (CHEI) and risk of diabetes in Chinese adults: a prospective cohort study.

PURPOSE: The Chinese Healthy Eating Index (CHEI) is a valid instrument to assess the diet quality of the Chinese population, but evidence regarding the relationship between CHEI and the risk of diabetes remains limited. We aimed to investigate the prospective association of CHEI with diabetes among Chinese adults. METHODS: 1563 adults free of diabetes at baseline and with at least two survey data from 1997 to 2018 were included. Dietary information was collected by three consecutive 24-h recalls combined with household food inventory, and long-term diet quality was evaluated by the CHEI. Diabetes was defined as self-reported physician-diagnosed diabetes and/or fasting blood glucose ≥ 7.0 mmol/L, and/or HbA1c ≥ 6.5%. Cox proportional hazard models and restricted cubic spline analysis were used to estimate the associations between CHEI and diabetes. RESULTS: During a median follow-up of 12.0 years, 192 (10.3%) participants developed new-onset diabetes. Generally, a five-point higher CHEI score was significantly associated with a 17% lower risk of diabetes (HR, 0.83; 95%CI 0.71-0.97). In stratified analysis, inverse associations between CHEI and diabetes were more vigorous in females (HR, 0.68; 95%CI 0.54-0.85) than in males (P for interaction = 0.01). In addition, there was an L-shaped association between CHEI and diabetes risk in the whole population (P for non-linearity = 0.026), while no significant non-linear association was observed in females or males, respectively. CONCLUSION: Our results suggested that a long-term higher-quality diet evaluated by CHEI was significantly associated with lower risks of diabetes, and the favorable associations were more pronounced among females.

Associations between dietary patterns and serum uric acid concentrations in children and adolescents: a cross-sectional study.

The serum uric acid (SUA) concentrations in children and adolescents in southeast coastal China are generally high. The relationship between diet and SUA in children and adolescents remains unclear. The objective of the study was to assess the associations between data-driven dietary patterns with SUA concentrations and hyperuricemia in Chinese children and adolescents and to explore the role of food components. This study involved 3383 participants aged 9 to 17 years from a representative nutrition and growth survey conducted in Shenzhen, a southeast coastal city in China. The dietary intake data, obtained from a validated food frequency questionnaire, were categorized into 19 food groups for factor analysis to derive dietary patterns. Weighted least squares regression was performed to examine the associations between dietary patterns and SUA concentrations, logistic regression was used to analyze the relationship between dietary patterns and hyperuricemia, and the relationship between food groups and food components with SUA concentrations was further analyzed. The potential dietary factors contributing to the associations between dietary patterns and SUA concentrations were explored by adjusting various food components. Six dietary patterns were identified by factor analysis, including an ultra-processed diet, plant-based nutritious diet, meat-based diet, soup/seafood/egg diet, vegetarian diet, and mushroom/animal organ diet. After adjusting for confounders, the meat-based diet exhibited a positive correlation with SUA concentrations (ß = 4.89; 95% confidence interval (CI): 0.60-9.18; P = 0.03), while the vegetarian diet could reduce the risk of hyperuricemia (odds ratio = 0.88; 95% CI: 0.80-0.98; P = 0.02). In addition, dietary intake of poultry (g per d) (ß = 0.09, 95% CI: 0.02, 0.16, P = 0.02), animal organs, blood (g per d) (ß = 0.32, 95% CI: 0.12, 0.51, P = 0.002) and hypoxanthine (mg per d) (ß = 0.03, 95% CI: 0.01, 0.06, P = 0.02) showed a significantly positive correlation with SUA concentrations, while that of vegetables (g per d) (ß = -0.02, 95% CI: -0.03, -0.01, P = 0.03) showed a significantly negative correlation. In summary, for children and adolescents, it is recommended to increase vegetable intake and reduce animal-based food intake in order to control SUA concentration and prevent hyperuricemia. This study was registered at the China Clinical Trials Registry (ChiCTR2100051722).

Biological aging mediates the associations between urinary metals and osteoarthritis among U.S. adults.

BACKGROUND: Osteoarthritis (OA) is a worldwide public health concern, mainly afflicting older adults. Although the etiology of OA remains unclear, environmental factors are increasingly considered as non-negligible risk factors. This study aims to evaluate the associations of urinary metals with OA risk and the mediated effect of biological aging. METHODS: Nine urinary metal concentrations were detected among 12,584 U.S. adults based on the National Health and Nutrition Examination Survey (NHANES), including barium (Ba), cadmium (Cd), cobalt (Co), cesium (Cs), molybdenum (Mo), lead (Pb), antimony (Sb), thallium (Tl), and uranium (Tu). Multivariable logistic regression and weighted quantile sum (WQS) regression were used to explore the associations of single metal and mixed metals with OA risk, respectively. Furthermore, biological aging was measured from different perspectives, including cell senescence (telomere length) and whole-body aging (phenotypic age and biological age). Mediation analyses were conducted to investigate the mediated effects of aging on the associations of metals with OA risk. RESULTS: In the single-exposure model, Cd, Co, and Cs were identified to be positively associated with OA risk, with odds ratios (OR) ranging from 1.48 to 1.64 (all P < 0.05). Mixed-exposure analyses showed consistent associations (OR 1.23, 95%CI 1.10 to 1.37) and highlighted that Cd, Co, and Cs were responsible for the outcomes. Additionally, Cd, Co, Cs, Pb, and Tl were positively associated with biological aging markers, while all biological aging markers had significant associations with OA risk. Further mediation analyses showed that the associations of single metal (mainly Cd and Cs) and mixed metals with OA risk parallelly mediated by the above biological aging markers, with the proportion of mediation ranging from 16.89 to 69.39% (all P < 0.05). Moreover, such associations were also serially mediated through telomere length-biological age path and telomere length-phenotypic age path (the proportion of mediation: 4.17-11.67%), indicating that metals accelerated cell senescence to lead to whole-body aging and finally aggravated OA progress. CONCLUSIONS: These findings suggested that exposure to metals increased OA risk, which was possibly and partly mediated by biological aging.

Whole-transcriptome analysis of aluminum-exposed rat hippocampus and identification of ceRNA networks to investigate neurotoxicity of Al.

Aluminum is a known neurotoxin that can induce Aß deposition and abnormal phosphorylation of tau protein, leading to Alzheimer disease (AD)-like damages such as neuronal damage and decreased learning and memory functions. In this study, we constructed a rat model of subchronic aluminum maltol exposure, and the whole-transcriptome sequencing was performed on the hippocampus of the control group and the middle-dose group. A total of 167 miRNAs, 37 lncRNAs, 256 mRNAs, and 64 circRNAs expression changed. The Kyoto Encyclopedia of Genes and Genomes showed that PI3K/AKT pathway was the most enriched pathway of DEGs, and IRS1 was the core molecule in the PPI network. circRNA/lncRNA-miRNA-mRNA networks of all DEGs, DEGs in the PI3K/AKT pathway, and IRS1 were constructed by Cytoscape. Molecular experiment results showed that aluminum inhibited the IRS1/PI3K/AKT pathway and increased the content of Aß and tau. In addition, we also constructed an AAV intervention rat model, proving that inhibition of miR-96-5p expression might resist aluminum-induced injury by upregulating expression of IRS1. In general, these results suggest that the ceRNA networks are involved in the neurotoxic process of aluminum, providing a new strategy for studying the toxicity mechanism of aluminum and finding biological targets for the prevention and treatment of AD.