Lipids in Health and Disease最新文献

Background: Nutritional status, recognized as a modifiable determinant of oral health, has recently gained increasing attention in the context of edentulism. The triglyceride-total cholesterol-body weight index (TCBI) is a novel nutritional indicator derived from routine clinical measures. However, its association with edentulism remains unclear. This study was designed to assess the association between TCBI and edentulism risk.

Methods: This study utilized survey data provided by the China Health and Retirement Longitudinal Study (CHARLS). Three analyses were performed: cross-sectional (n = 9,686), prospective (participants without baseline edentulism, n = 8,568), and trajectory analyses (TCBI trajectories and incident edentulism, n = 4,921). Logistic regression, Cox proportional hazards models, group-based trajectory modeling, and restricted cubic spline analyses were applied. Sensitivity analyses using cumulative TCBI during follow-up were also conducted.

Results: In the cross-sectional analysis, individuals in the highest TCBI tertile demonstrated a significantly lower risk of prevalent edentulism (adjusted OR = 0.80, 95% CI: 0.65-0.97). In the prospective analysis, higher TCBI levels were independently associated with a reduced risk of incident edentulism (adjusted HR = 0.85, 95% CI: 0.77-0.92). Trajectory modeling demonstrated that individuals with persistently high TCBI had the lowest risk of incident edentulism (adjusted HR = 0.59, 95% CI: 0.40-0.89). These associations remained robust in sensitivity analyses.

Conclusion: TCBI was consistently and inversely associated with edentulism across cross-sectional, prospective, and trajectory analyses. As a readily obtainable nutritional index, TCBI may have clinical utility for the early identification and risk prediction of edentulism.

Background: The connection between low-density lipoprotein cholesterol (LDL-C) levels and postoperative outcomes following cardiac valve surgery (CVS) remains controversial. Therefore, this research aimed to study the connection of LDL-C levels with the incidence of adverse clinical outcomes in patients undergoing CVS.

Methods: 1,304 patients undergoing first-time CVS were identified from the MIMIC-IV database. Participants were split into two groups based on admission LDL-C levels: a low LDL-C group (< 1.4 mmol/L, n = 215) as well as a high LDL-C one (≥ 1.4 mmol/L, n = 1,089). The main endpoint was 30-day all-cause mortality (ACM), with secondary endpoints including in-hospital, 90-, 180- and 365-day ACM rates. The connection between preoperative LDL-C levels and clinical outcomes was evaluated via survival analysis, mediation analysis, and subgroup analyses.

Results: Multivariable Cox regression analysis demonstrated preoperative LDL-C level served as an independent protective factor against 30-day ACM following cardiac valve surgery (adjusted HR: 0.594; 95% CI: 0.368-0.960). In stratified analysis, patients in the higher LDL-C tertile exhibited a remarkably lower mortality risk (HR: 0.285; 95% CI: 0.134-0.604). Consistent subgroup analyses validated these findings' robustness across all clinically relevant subgroups. Notably, mediation analysis provided mechanistic evidence that the mortality-increasing effect of lower LDL-C levels may be partially mediated through activation of systemic inflammation.

Conclusion: Lower preoperative LDL-C levels are independently related with higher 30-day mortality following cardiac valve surgery, potentially mediated by the activation of inflammatory pathways.

Background: Vascular calcification (VC) is highly prevalent in patients undergoing maintenance hemodialysis (MHD) and is associated with cardiovascular morbidity. However, traditional lipid and mineral markers have limited predictive value. Y-box binding protein-1 (YB-1), a regulator of lipid metabolism and inflammation, may provide additional mechanistic and clinical insight.

Methods: Serum YB-1 was measured in 209 MHD patients (30-month follow-up) who were stratified into hyperlipidemia and control groups. Receiver Operating Characteristic (ROC) and decision curve analysis (DCA, threshold range 0.1-0.4) were used to assess the predictive performance of YB-1 against traditional models based on lipid, glucose, and bone metabolism. Mechanistic studies in HL-60-derived neutrophil-like cells and a 5/6 nephrectomized rat model were performed to assess the role of YB-1 in neutrophil extracellular trap (NET) formation and VC.

Results: Serum YB-1 was significantly elevated in hyperlipidemia patients and was independently associated with new-onset VC (AUC 0.707, 95% CI 0.630-0.784). YB-1 outperformed lipid-, glucose-, and bone-based models, providing added net clinical benefit in DCA within the 0.24-0.33 threshold range. Mechanistically, serum levels of citrullinated histone H3 (citH3), a NET marker, were increased in hyperlipidemia patients. In vitro, YB-1 and IS synergistically enhanced neutrophil lipid droplet accumulation and citH3 release, while NET-rich supernatants promoted VSMC calcification. In vivo, IS-treated 5/6 nephrectomy rats displayed elevated YB-1, increased citH3, and aggravated aortic calcification.

Conclusion: Serum YB-1 is a novel predictor and potential mechanistic mediator of VC in MHD patients. Incorporating YB-1 into existing clinical risk models may support earlier recognition of individuals at elevated cardiovascular risk and inform more effective management strategies to improve long-term health outcomes.

Background: Lipids play crucial roles in maternal and foetal metabolism; however, their effects on birth weight remain unclear. Moreover, the potential mediating role of inadequate gestational weight gain (iGWG) in this association remains unexplored. The objective of this study was to assess maternal lipid profiles in the third trimester and their associations with the risk of small-for-gestational-age (SGA) infants, focusing on the combined effects of high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG). This study also examined whether iGWG influenced this relationship.

Methods: Data were sourced from the Tongji Maternal and Child Health Cohort. Maternal fasting lipid levels were measured during the third trimester and birth information was retrieved from medical records. Log-Poisson regression analysis was performed to assess the relationship between lipid tertiles and SGA risk. The possible mediating role of iGWG was examined using the mediation package in R.

Results: An increased risk of SGA was associated with high HDL-C levels (adjusted relative risk [aRR], 1.54; 95% confidence interval [CI], 1.15-2.07), particularly among mothers with high HDL-C and low TG levels (aRR, 1.77; 95% CI, 1.10-2.87). This association remained significant among individuals with normal pre-pregnancy weight. The relationship between lipid profiles and SGA was independent of iGWG.

Conclusions: An increased risk of SGA was associated with high maternal HDL-C levels. The combination of low TG and high HDL-C levels was identified as a significant predictor of SGA. iGWG did not explain these associations.

Diabetic kidney disease (DKD), the predominant microvascular complication of diabetes mellitus, perpetuates a significant global health and socioeconomic challenge, complicating the pursuit of sustainable renal care. Adipokines, bioactive proteins secreted by adipose tissue that modulate lipid metabolism, function as key modulators potentially integrating systemic metabolic and inflammatory signals with renal pathophysiology Mechanistic investigations reveal that adipokines orchestrate a range of interconnected pathways, which include metabolic dysregulation (characterized by insulin resistance and lipid overload), immune-inflammatory responses (mediated by nuclear factor kappa B [NF-κB], NLR family pyrin domain containing 3 [NLRP3], and chemokine axes), oxidative stress coupled with mitochondrial dysfunction (involving adenosine monophosphate-activated protein kinase [AMPK] and peroxisome proliferator-activated receptor gamma coactivator 1-alpha [PGC-1α], reactive oxygen species [ROS]), endothelial dysfunction, fibrogenesis (driven by transforming growth factor beta [TGF-β]/Smad and epithelial-mesenchymal transition [EMT]), and the imbalance between apoptosis and autophagy. Protective adipokines such as adiponectin, irisin, and vaspin may mitigate harmful signaling, whereas leptin, resistin, visfatin, and chemerin could amplify injury through pro-inflammatory, pro-fibrotic, and lipotoxic pathways. Both circulating and urinary levels of adipokines may correlate with proteinuria, which suggests their potential utility in early detection, risk stratification, or therapeutic monitoring, although further validation is required.Emerging pharmacological, genetic, and lifestyle interventions may modulate adipokine networks to confer renal protection. The integration of multi-omics approaches, single-cell analysis, and spatial profiling with models that closely mimic human physiology is essential for identifying key signaling nodes, validating biomarkers, and developing precision-targeted therapies. Collectively, a detailed, network-oriented understanding of lipid-regulating adipokines could support efforts toward the development of personalized prevention and treatment strategies in DKD.

Background: Cardiometabolic multimorbidity (CMM) poses a major health burden in aging populations. The long-term effect of cumulative remnant cholesterol inflammatory index (RCII) on CMM remains unclear. This study aimed to examine this relationship among middle-aged and older Chinese adults.

Methods: This retrospective longitudinal cohort included 5,150 participants aged ≥ 45 years without baseline CMM from the China Health and Retirement Longitudinal Study. The cumulative average natural log-transformed RCII (cumlnRCII) was calculated from 2011 to 2015. RCII was defined as (remnant cholesterol × high-sensitivity C-reactive protein)/10. Incident CMM was defined as the new onset of at least two of the following conditions: diabetes, heart disease, or stroke by 2018. Multivariate Cox and logistic models were used to estimate the hazard ratio (HR) and odds ratio (OR), with restricted cubic splines used to test dose-response relationships. Subgroup and sensitivity analyses were conducted to ensure the reliability of the results.

Results: Over a median follow-up period of 7 years, 294 participants developed CMM. The incidence of CMM increased across cumlnRCII tertiles: 3.2% (Tertile 1), 5.2% (Tertile 2), and 8.7% (Tertile 3). After adjustment, compared with Tertile 1, Tertile 3 had significantly greater risks (OR = 2.14, 95% CI: 1.55-2.99; HR = 2.10, 95% CI: 1.53-2.89). Each 1-standard deviation increase in cumlnRCII was associated with a 33% higher odds and a 32% higher risk of CMM. A linear dose-response correlation was identified (P-nonlinear = 0.383). Most subgroups exhibited consistent associations, and sensitivity analyses validated the reliability of the results.

Conclusions: The cumulative average RCII is independently associated with increased CMM risk, underscoring its value for identifying high-risk individuals, guiding preventive strategies, and advancing efforts toward healthy aging by reducing the burden of cardiometabolic disease.