Lipids最新文献

The relationship between primary aldosteronism (PA) and lipid metabolism remains controversial, with inconsistent findings reported in the literature. This study aimed to clarify PA's impact on the lipid profile using both a cross-sectional comparison with essential hypertension (EH) controls and a longitudinal within-patient pre-post treatment analysis in a North African tertiary-center cohort. This retrospective study included 112 patients with PA and 115 contemporaneously hospitalized patients with EH in whom secondary hypertension had been excluded. Sociodemographic, clinical, and biochemical variables (fasting blood glucose, HbA1c, lipid profile, creatinine, potassium, baseline aldosterone levels, and aldosterone-to-renin ratio), as well as therapeutic data, were collected at admission in both groups. In the PA group, clinical and biological parameters performed 1 year after specific PA management were recorded. Triglyceride levels were significantly higher in patients with PA not receiving lipid-lowering therapy (1.47 (1.13-1.92) vs. 1.24 (1.02-1.69) mmol/L; p = 0.04) but this difference disappeared after multivariable adjustment for age, sex, BMI, and fasting glucose. A baseline aldosterone level > 200 pg/mL was associated with lower triglyceride levels (1.35 (1.02-1.81) vs. 1.81 (1.35-2.15) mmol/L; p = 0.01). Patients with PA who underwent adrenalectomy demonstrated a significant increase in triglyceride levels at 1 year (1.52 (1.32-2.11) vs. 2.08 (1.38-2.50) mmol/L; p = 0.04). The estimated glomerular filtration rate declined significantly 1 year after PA specific treatment (84.9 ± 19.7 vs. 73.6 ± 24.9 mL/min/1.73 m²; p < 0.01). Our findings show mixed associations between aldosterone and triglyceride levels, which require confirmation in prospective studies.

Cardiovascular diseases (CVD) are a leading cause of global mortality, with dyslipidemia playing a central role in their pathogenesis. The influence of alcohol consumption on lipid profiles, particularly high-density lipoprotein cholesterol (HDL-c), in relation to obesity status remains insufficiently explored. We evaluated the association between alcohol consumption and HDL-c levels in individuals with and without obesity in a Brazilian population. This cross-sectional analysis used data from the Baependi Heart Study, comprising 2345 participants aged 18-100 years. Alcohol intake was categorized according to weekly ethanol consumption, and HDL-c levels were measured through standard biochemical methods. No significant differences were observed across alcohol consumption groups for total cholesterol, LDL-c, triacylglycerols, and fasting glucose; however, the HDL-c/LDL-c ratio was significantly higher among male moderate consumers. A significant interaction was found between obesity and moderate alcohol consumption (β = 0.90, p = 0.015), indicating that the relationship between alcohol intake and low HDL-c varies according to obesity status. Moderate alcohol consumers exhibited significantly higher HDL-c levels compared to abstainers, an association observed exclusively among nonobese participants. In this group, moderate alcohol intake was linked to a 65% reduction in the odds of low HDL-c in women and a 66% reduction in men. No significant association was observed among individuals with obesity. Moderate alcohol consumption was associated with higher HDL-c levels and lower odds of low HDL-c, particularly among individuals without obesity. These findings contribute to the understanding of the complex interplay between alcohol intake, lipid metabolism, and adiposity.

Long chain polyunsaturated fatty acids are an important determinant of the birth weight of the baby. Studies have reported altered fatty acid desaturase indices (Δ5 and Δ6 desaturases) from early pregnancy in women with pregnancy complications. However, it remains unclear if these alterations are also observed in women who have no complications, yet delivering low birth weight (LBW) infants (birth weight below 2500 g regardless of gestational age). This study aims to longitudinally examine the maternal erythrocyte fatty acids levels in women delivering LBW babies (in women with pregnancy complications and without complications) and in women delivering normal birth weight babies (NBW). This study includes 1096 singleton pregnant women, out of which 181 delivered LBW babies. Maternal erythrocyte fatty acids were measured at 11-14 weeks, 18-22 weeks, and 26-28 weeks and at delivery using gas chromatography. Product-precursor ratios were used to represent enzyme indices: Δ5D index = arachidonic acid/dihomo-y-linolenic acid (DGLA), Δ6D index = DGLA/linoleic acid. Maternal age at the time of delivery was: NBW group: 28.74 ± 4.65; LBW group: 28.14 ± 4.61 and LBW without complications group: 26.99 ± 4.20. Birth weight of the baby was: NBW: 2978.69 ± 340.37; LBW: 2404.47 ± 262.85; LBW without complications group: 2308.02 ± 202.06. Higher Δ5 desaturase and lower Δ6 desaturase indices at 11-14 weeks of gestation were associated with higher risk of having LBW babies (p < 0.01 for both). This study reports that disrupted fatty acid metabolism in early pregnancy regardless of pregnancy complications is a risk factor for having LBW babies.

This study aimed to evaluate whether the neutrophil-to-high-density lipoprotein cholesterol ratio (NHR) is independently associated with Insulin Resistance (IR) among individuals with obesity and to examine the robustness of this association across distinct populations. Two independent cohorts were analyzed: a Chinese training cohort (n = 764) and a US validation cohort from the National Health and Nutrition Examination Survey (NHANES; n = 2963). Multivariable logistic regression and restricted cubic spline (RCS) models were applied to assess associations between NHR and IR. Subgroup analyses evaluated consistency, and receiver operating characteristic (ROC) curves assessed predictive performance. NHR was positively associated with IR in both cohorts. After full adjustment, each unit increase in NHR was associated with a 23% higher IR risk in the training cohort (OR = 1.23, 95% CI: 1.10-1.38) and a 21% higher risk in the validation cohort (OR = 1.21, 95% CI: 1.09-1.35). Participants in the highest NHR quartile had markedly increased IR risk compared with the lowest quartile (training: OR = 4.45, 95% CI: 2.27-8.69; validation: OR = 2.04, 95% CI: 1.37-3.03). RCS analysis indicated a linear association in the training cohort and a nonlinear pattern in the validation cohort. Associations were consistent across subgroups. NHR showed modest predictive ability (AUC: 0.677 and 0.654). NHR demonstrated a significant positive association with insulin resistance in Chinese and US obese cohorts, indicating its potential utility as a biomarker for IR and associated diseases.

Background: Post-transplant diabetes mellitus (PTDM) is a common complication following liver transplant (LT) and is associated with adverse outcomes. The triacylglycerol-glucose product (TyG) and the triacylglycerol-to-high-density lipoprotein (HDL) cholesterol ratio (TAG/HDL-c) are indices that can serve as triacylglycerol-based proxies for insulin resistance. Their relation to PTDM in liver-transplant recipients (LTRs) is unclear.

Methods: TyG and TAG/HDL-c (nuclear magnetic resonance spectroscopy) were compared between LTRs without diabetes at baseline and participants without diabetes from the community-dwelling PREVEND cohort. Among LTRs, associations with incident PTDM were determined using Cox regression analysis and logistic regression analysis with adjustment for relevant variables.

Results: TyG was higher in 246 LTRs without diabetes (mean age 52.6 years; 53.7% male) compared to 4533 PREVEND participants without diabetes (mean 53.1 years; 48.9% male (p < 0.001), and confirmed using propensity score matching (p < 0.001). Over a median follow-up of 7.1 (IQR 6.2-7.8) years, 31 LTRs developed PTDM (12.6% cumulative incidence). A higher baseline TyG index was associated with an increased risk of PTDM (HR per 1-SD increase: 1.67, 95% CI 1.28-2.30; highest vs. lowest tertile HR: 1.77, 95% CI 1.14-2.64). The TAG/HDL-c ratio followed the same trend (HR per 1-SD increase: 1.56, 95% CI 1.14-2.15; highest vs. lowest tertile: HR 3.80, 95% CI 1.73-10.0). Findings remained in adjusted analyses and were directionally similar in logistic regression models.

Conclusions: In LTRs, both the TyG index and the TAG/HDL-c ratio are associated with PTDM. These indices could serve as a basis for post-transplant risk stratification in diabetes development.

The triglyceride glucose (TyG) index is increasingly recognized as a simple yet reliable surrogate marker of insulin resistance. This study aimed to explore the relationship between the TyG index and liver fat content (LFC) quantified via quantitative computed tomography (QCT) in individuals with type 2 diabetes mellitus (T2DM). This cross-sectional analysis included patients with T2DM who underwent QCT examinations at our institution between January and December 2024. QCT was used to measure tissue components at the mid-L2 vertebral level, including subcutaneous fat area (SFA), visceral fat area (VFA), and LFC. A multiple linear regression model was employed to assess the independent association between the TyG index and LFC. The study enrolled 168 participants, comprising 112 males and 56 females. Subjects in the highest TyG index tertile exhibited a more adverse cardiometabolic risk profile and higher LFC compared to those in the lowest tertile. Correlation analyses indicated that the TyG index was significantly associated with both SFA and LFC. After adjusting for age and gender, multiple linear regression confirmed that the TyG index remained independently and positively associated with LFC (β = 1.73, 95% CI: 0.08-3.38, p = 0.042). Stratified analyses revealed that the positive association between the TyG index and LFC was consistent across all strata, with no significant interactions observed for age, gender, duration of T2DM, and body mass index. Our findings suggest that the TyG index may serve as a reliable, noninvasive surrogate marker for evaluating LFC in individuals with T2DM.

The non-high-density lipoprotein cholesterol (non-HDL-c) to high-density lipoprotein cholesterol (HDL-c) ratio (NHHR) is an emerging and valuable biomarker for cardiovascular disease risk. Nevertheless, robust evidence regarding its relationship with both the prevalence and severity of albuminuria remains incompletely elucidated. This cross-sectional study analyzed data from the 1999 to 2018 US National Health and Nutrition Examination Survey to investigate the association between NHHR and albuminuria, assessed via the urinary albumin-to-creatinine ratio (uACR). Multivariate logistic and linear regression models, restricted cubic spline analysis, subgroup analyses and receiver-operating characteristic curve analysis were employed. Among the 14,376 participants included, the prevalence of microalbuminuria and macroalbuminuria was 6.83% and 1.06%, respectively. The adjusted odds ratios (95% confidence intervals) for each one-unit increase in NHHR were 1.09 (1.04-1.15) for any albuminuria, 1.06 (1.01-1.12) for microalbuminuria, and 1.23 (1.11-1.37) for macroalbuminuria. NHHR was positively correlated with uACR (β = 4.08, 95% confidence interval 1.11-7.04). Restricted cubic spline analysis revealed a positive association, which became more pronounced at NHHR levels exceeding 2.77. Subgroup analyses further demonstrated that this association was stronger in individuals with a body mass index ≥ 30 kg/m² or an estimated glomerular filtration rate ≥ 90 mL/min/1.73 m². Receiver-operating characteristic curve analysis confirmed that NHHR possessed superior discriminative power for albuminuria compared to conventional lipid parameters of total cholesterol, HDL-c, non-HDL-c, triglycerides, and apolipoprotein B. We concluded that elevated NHHR is positively and independently associated with an increased risk and severity of albuminuria, highlighting its clinical relevance as a potential biomarker, particularly among individuals with obesity and preserved renal function.

The precise involvement of ACSL1 in metabolic-associated fatty liver disease (MAFLD) pathogenesis remains unclear. To this end, we analyzed the effects of long-chain acyl-CoA synthase (ACSL1) on MAFLD. Analysis of GEO datasets showed that ACSL1 was downregulated in MAFLD. To elucidate its mechanistic role, we generated BRL hepatocyte cell lines with stable ACSL1 knockdown or overexpression. These engineered cells were cultured with a lipid mixture containing 300 μM oleic acid, 150 μM palmitic acid, and 100 μM linoleic acid (OPL) to mimic MAFLD pathophysiology in vitro. Lipidomic profiling identified 195 upregulated and 357 downregulated lipid metabolites in OPL-treated ACSL1-knockdown cells (OPL-shACSL1). Notably, the OPL-shACSL1 group exhibited marked elevations in free fatty acids, including linoleic acid, arachidonic acid (AA), FA20:3, FA22:5, and FA22:2, accompanied by enhanced AA metabolism. Western blotting demonstrated that ACSL1 knockdown significantly upregulated key enzymes in AA metabolic pathways, including ELOVL5, COX1, and LOX5. Consistent with these in vitro findings, mice with high-fat diet-induced MAFLD showed reduced hepatic ACSL1 expression with concurrent elevation of COX1 protein levels. Co-immunoprecipitation assays showed that ACSL1 did not interact with LOX5 or COX1. Our findings demonstrate that ACSL1 knockdown enhances AA metabolism, evidenced by elevated levels of AA-related metabolites and upregulated expression of key enzymes (ELOVL5, COX1, LOX5), and suggest that ACSL1 may represent a potential therapeutic target for MAFLD.

To examine the disparities in adipose tissue browning between diets rich in lard and soybean oil under low and recommended caloric intake conditions. In this study, sixty 8-week-old male C57BL/6J mice were randomly divided into four groups fed purified diets with 15% and 25% energy provided as lard or soybean oil. After 20 weeks, the mice were dissected and the tissues were collected. Only at the 25% level was there a significant difference in the brown adipose tissue between the two groups of mice fed different oils. The expression of mRNA related to the BAT was tested by qPCR methods. Diversity of microbiota in cecal content was evaluated by the 16S rRNA sequencing. Compared with soybean oil, the BAT weight of the lard group was significantly increased (p < 0.05), and the protein expression of UCP1 in iWAT was significantly higher (p < 0.05). The expression levels of adipose browning, thermogenesis and mitochondria genes were significantly increased in the lard group, and lipogenesis-related genes were significantly decreased (p < 0.05). The proportions of Akkermansia, Romboutsia, Lactobacillus, and Streptococcus were significantly increased in the lard group (p < 0.05). This study suggests that at the dietary fat energy level of 25%, feeding with lard could promote the browning of fat, improve lipid metabolism, and increase the abundance of beneficial bacteria in the gut.

Chronic low-grade inflammation contributes to aging, metabolic dysfunction, and age-related diseases. High-sensitivity C-reactive protein (HsCRP) is widely used but limited by short-term variability. DNA methylation-based CRPMort derived from GrimAge2 may provide a more stable measure of chronic inflammatory burden, yet its predictive value for mortality and association with lipid metabolism remain unclear. Associations of CRPMort and HsCRP with all-cause and cardiovascular mortality and lipid traits were evaluated using weighted cox regression and linear regression, Kaplan-Meier curves, restricted cubic splines (RCS), and time-dependent receiver operating characteristic curve (timeROC) analyses within the NHANES database, with subgroup, mediation, sensitivity, and Mendelian randomization analyses. Higher CRPMort was significantly associated with all-cause mortality (hazard ratio [95% confidence interval]: 1.65 [1.10, 2.46], p = 0.015) and showed near-significant positive associations with triglycerides (p = 0.051) and residual cholesterol (p = 0.056). RCS analyses demonstrated a linear positive relationship between CRPMort and both all-cause mortality and lipid traits, including triglycerides and residual cholesterol. HsCRP showed no significant associations with mortality or lipid traits (all p > 0.05). TimeROC curves revealed that compared to HsCRP, CRPMort had more superior long-term predictive performance and partially mediated the effect of chronological age on all-cause mortality. Importantly, concurrent elevations of CRPMort and HsCRP were associated with the highest risks of all-cause mortality and dyslipidemia. GrimAge2-derived CRPMort is a robust predictor of long-term all-cause mortality and may capture chronic inflammation linked to triglyceride-rich lipoproteins beyond HsCRP. Combined assessment of both inflammatory markers may enhance risk stratification and inform aging-related cardiometabolic research.