Shoumeng Yan

Background: Dyslipidemia is one of the most common chronic diseases, and is associated with insulin resistance (IR) and inadequate vitamin K intake. We aimed to explore the association between IR, vitamin K intake, and dyslipidemia, and further to explore the mediating role of IR. Materials and methods: 12 860 participants from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2018 were included in this study. Insulin resistance was determined by using the homeostatic model assessment for insulin resistance (HOMA-IR). Weighted multiple logistic regression and mediation analyses were conducted to analyze the associations between IR, vitamin K intake, and dyslipidemia. Results: We found that both vitamin K intake-met Dietary Reference Intake (DRI) and non-IR were protective factors of high triglycerides (with ORs (95% CI) of 0.71 (0.57, 0.87) and 0.36 (0.29, 0.45), respectively) and low high-density lipoprotein cholesterol (with ORs (95% CI) of 0.72 (0.62, 0.82) and 0.39 (0.34, 0.41), respectively). IR-related indicators (HOMA-IR and insulin) partly mediated these effects, and the proportion ranged from 16.36% to 18.52%. Conclusion: Vitamin K intake-met DRI and non-IR were associated with lower risk of dyslipidemia including high TG and low HDL-C. IR partly mediated the association of vitamin K intake with high TG and low HDL-C.

Background: Precocious puberty, one of the common pediatric endocrine system diseases, has been related to reduced adult height, adverse psychological outcomes and long-term health consequences. Previous findings have found that low levels of vitamin D appear to be associated with the characteristics of precocious puberty such as early menarche. However, the effect of vitamin D on precocious puberty remains controversial. Methods: The published literature was searched from PubMed, Web of Science, Cochrane Library, MEDLINE, EMBASE, CNKI, Wan Fang and VIP databases up to October 2022. A randomized effect model was used to perform a meta-analysis to evaluate differences in vitamin D concentration between precocious puberty subjects and normal subjects, the risk of precocious puberty in subjects with low vitamin D levels, and the effect of supplementation of vitamin D on subjects with precocious puberty on medication. Results: Our study found that precocious puberty subjects had lower serum vitamin D levels than the normal population (standardized mean difference (SMD) = −1.16 ng ml⁻¹ and 95% confidence interval (CI) = −1.41 and −0.91 ng ml⁻¹). Meanwhile, the lower level of vitamin D was associated with the risk of precocious puberty (odd ratio (OR) = 2.25 and 95% CI = 1.66 and 3.04). Moreover, compared with gonadotropin-releasing hormone analogue (GnRHa) intervention alone, subjects receiving GnRHa + vitamin D intervention had significantly lower luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estradiol levels and bone age, and higher predicted adult height (PAH). Conclusions: Vitamin D may have a potential role in precocious puberty and more data from large clinical trials are needed to confirm the findings.

Compared with diabetic patients with normal blood lipid, diabetic patients with dyslipidemia such as high triglycerides have a higher risk of clinical complications, and the disease is also more serious. For the subjects with hypertriglyceridemia, the lncRNAs affecting type 2 diabetes mellitus (T2DM) and the specific mechanisms remain unclear. Transcriptome sequencing was performed on peripheral blood samples of new-onset T2DM (six subjects) and normal blood control (six subjects) in hypertriglyceridemia patients using gene chip technology, and differentially expressed lncRNA profiles were constructed. Validated by the GEO database and RT-qPCR, lncRNA ENST00000462455.1 was selected. Subsequently, fluorescence in situ hybridization (FISH), real-time quantitative polymerase chain reaction (RT-qPCR), CCK-8 assay, flow cytometry, and enzyme-linked immunosorbent assay (ELISA) were used to observe the effect of ENST00000462455.1 on MIN6. When silencing the ENST00000462455.1 for MIN6 in high glucose and high fat, the relative cell survival rate and insulin secretion decreased, the apoptosis rate increased, and the expression of the transcription factors Ins1, Pdx-1, Glut2, FoxO1, and ETS1 that maintained the function and activity of pancreatic β cells decreased (p < 0.05). In addition, we found that ENST00000462455.1/miR-204-3p/CACNA1C could be the core regulatory axis by using bioinformatics methods. Therefore, ENST00000462455.1 was a potential biomarker for hypertriglyceridemia patients with T2DM.

The underlying mechanism in both cognitive impairment and depression was chronic inflammation, which could be reflected by the dietary inflammatory index (DII). However, the effect of cognitive impairment on the association between DII and depression was not clear. Therefore, in this study, we hypothesized that cognitive impairment could mediate the association between dietary inflammation and depressive symptoms. A total of 2550 participants aged ≥60 from the National Health and Nutrition Examination Survey (NHANES) in 2011–2014 were involved in the serial, cross-sectional study. Proinflammatory and anti-inflammatory diets were measured by DII. Cognitive impairment was measured by four dimensions, CERAD-immediate, CERAN-delayed, animal fluency test, and DSST. Depressive symptoms were measured by PHQ-9 scores. We found that a proinflammatory diet and cognitive impairment were both risk factors for depressive symptoms. An interaction between an inflammatory diet and cognitive impairment was detected (P-interaction = 0.060). In addition, all four dimensions of cognition mediated the association between DII and depressive symptom scores. Part of the association between DII and depressive symptoms scores could be explained by different dimensions of cognitive function, and the proportion of mediation ranged from 10.0% to 36.7%. In conclusion, cognitive impairment levels partly mediated the association between DII and depressive symptoms.

Metabolic dysfunction-associated fatty liver disease (MAFLD) has been related to a series of harmful health consequences. The triglyceride-glucose index (TyG index) appears to be associated with MAFLD. However, no consistent conclusions about the TyG index and incident MAFLD have been reached. PubMed, MEDLINE, Web of Science, EMBASE and the Cochrane Library were searched. Sensitivities, specificities and the area under the receiver operating characteristic (AUC) with a random-effects model were used to assess the diagnostic performance of the TyG index in NAFLD/MAFLD participants. Potential threshold effects and publication bias were evaluated by Spearman’s correlation and Deeks’ asymmetry test, respectively. A total of 20 studies with 165725 MAFLD participants were included. The summary receiver operator characteristic (SROC) curve showed that the sensitivity, specificity and AUC were 0.73 (0.69–0.76), 0.67 (0.65, 0.70) and 0.75 (0.71–0.79), respectively. Threshold effects (r = 0.490, p < 0.05) were confirmed to exist. Subgroup analyses and meta-regression showed that some factors including country, number of samples, age and disease situation were the sources of heterogeneity (p < 0.05). Our meta-analysis suggests that the TyG index can diagnose and predict MAFLD patients with good accuracy. The number of studies remains limited, and prospective studies are needed.