Lipids最新文献

The aim of this study was to investigate the association between lipid levels and mortality in individuals hospitalized (ward/intensive care unit) for coronavirus disease 2019 (COVID-19). This retrospective cohort study was conducted with COVID-19 patients admitted to a public hospital between April 2020 and 2021. Age, sex, and chronic disease status of the participants were analyzed as general information. Information on biochemical tests (high-density lipoprotein [HDL], low-density lipoprotein [LDL], triglycerides, total cholesterol, c-reactive protein [CRP]) and haemogram parameters were obtained from the hospital's automated system. The study sample consisted of 501 COVID-19 patients aged 24–94 years. According to mortality status, total cholesterol, HDL, LDL, and lymphocyte levels were higher, while CRP, neutrophil, and white blood cell levels were lower in survivors (p < 0.05). The risk of mortality was found to be higher with lower LDL and HDL cholesterol levels in COVID-19 patients (p < 0.05). The results of this study showed that alterations in lipoprotein metabolism are associated with mortality in COVID-19 patients. Therefore, it is important to evaluate and monitor the blood lipid profile in COVID-19 patients.

Various methods exist for identifying and quantifying lipid unsaturation, including mass spectrometry and Raman spectroscopy. A disadvantage of these existing approaches is the need for sophisticated equipment and software, placing them beyond the means of many laboratories. The iodine value (IV) is a colorimetric unsaturation index; however, it uses iodine monochloride, a hazardous chemical, and considerable amounts of sample. Here, we demonstrate the first use of a miniaturized IV method that requires only milliliter quantities of hazardous chemicals and sample sizes such that it is feasible to assay biological membranes. Briefly, lipids are exposed to iodine monochloride, resulting in the replacement of unsaturated bonds with di-halogenated single bonds. Potassium iodide then reacts with unreacted iodine monochloride forming I₂, which is quantified through titration with sodium thiosulfate. To demonstrate the biological relevance of our assay, membrane lipids of Escherichia coli grown at 30, 37, and 42°C were analyzed, with IV increasing as temperature decreased, as would be expected. Importantly, multiple samples could be rapidly and simultaneously analyzed in a reproducible assay that did not require sophisticated equipment or data analysis methods. Our miniaturized IV assay will benefit laboratories with limited access to sophisticated equipment and enable the rapid determination of lipid unsaturation in milligram-scale samples.

Rheumatic heart valvular disease (RHVD) is primarily characterized by immune-mediated damage following infection with Streptococcus pyogenes, leading to inflammation and subsequent valvular dysfunction. Traditionally, the focus has been on the immunological aspects of this disease; however, emerging evidence suggests that lipoprotein(a) [Lp(a)] may play a crucial role not only in atherosclerosis but also in the pathophysiology of calcific aortic valve disease. Given the inflammatory nature of RHVD and the pro-inflammatory and pro-calcific properties of Lp(a), this study aimed to investigate the relationship between serum Lp(a) levels and the severity of RHVD. In this cross-sectional study, we included 40 RHVD patients and 40 age- and sex-matched controls. Serum Lp(a) analysis was performed in all patients. We analyzed demographic and echocardiographic parameters and the relationship between serum Lp(a) concentrations and echocardiographic parameters. The mean age of the patient population was 50 ± 11 years and 47 (72%) were female. Lp(a) was higher in the RHVD group than in the control group (21 [19–49] vs. 17 [12–19] mg/dL; p < 0.001). Serum Lp(a) correlated positively with left atrial diameter (rho = 0.438; p = 0.005), estimated pulmonary artery systolic pressure (rho = 0.390; p = 0.019), Wilkins score (rho = 0.482; p = 0.002), number of valves involved (rho = 0.397; p = 0.011), aortic regurgitation grade (rho = 0.373; p = 0.018) and negatively correlated with mitral valve area (rho = −0.413; p = 0.008). In conclusion, serum Lp(a) concentrations were higher in patients with RHVD than in the control group and were positively correlated with disease severity indicators, including mitral stenosis grade, Wilkins score, aortic regurgitation grade, left atrial diameter, and estimated pulmonary artery systolic pressure.

Triacylglycerol (TG) is categorized into long-, medium-, and short-chain TG (SCTG). While the digestion of long- and medium-chain TG is well established, the process for SCTG remains unclear. This study investigated SCTG digestion by administering 2 mmol of triacetin to rats and analyzing acetin, acetic acid, and glycerol levels in the portal blood and small intestine. Triacetin was fully degraded in the upper gastrointestinal tract and absorbed as acetic acid and glycerol. Glycerol influx into the liver promoted gluconeogenesis, while acetate activated AMPK, resulting in the suppression of fatty acid synthesis-related genes and the upregulation of fatty acid β-oxidation-related genes. These findings demonstrate that triacetin not only serves as a substrate for energy metabolism but also regulates hepatic gene expression, highlighting its dual role as both a metabolic substrate and signaling molecule. Triacetin thus shows potential as a dietary modulator for improving metabolic health.

Lipid-lowering drugs have been used in clinics widely. It is unclear whether the drugs have an effect on renal failure. We chose high-density lipoprotein cholesterol (ieu-b-109), low-density lipoprotein cholesterol (ieu-a-300), triglyceride (ieu-b-111), and total cholesterol (ebi-a-GCST90038690) as exposures. SNPs near drug genes served as instrumental variables. Acute renal failure (ARF) and chronic renal failure (CRF) in Europeans from the GWAS catalog were selected as outcomes. Datasets on renal failure in East Asians and South Asians were used for validation. Inverse variance weighted (IVW) was the primary method for drug-targeted Mendelian randomization. In the Europeans, people who used PPARG reduced ARF risk by 69.3% (OR: 0.307, 95% CI: 0.171–0.553, p = 0.015). NPC1L1 inhibitors increased ARF risk by 2.684 times (OR: 2.684, 95% CI: 2.027–3.341, p = 0.003). APOE increased ARF risk by 1.987 times (OR: 1.987, 95% CI: 1.062–3.716, p = 0.032) but decreased CRF risk by 49.7% (OR: 0.503, 95% CI: 0.283–0.894, p = 0.019). TNFSF12 increased CRF risk by 3.866 times (OR: 3.866, 95% CI: 1.174–12.729, p = 0.026). In the East Asians, PPARG reduced CRF risk by 85.8% (OR: 0.142, 95% CI: 0.054–0.371, p < 0.001). And in the South Asians, APOE decreased ARF risk by 99.8% (OR: 0.002, 95% CI: 2.12e-05-0.179, p = 0.007). We revealed that PPARG could reduce the risk of renal failure in Europeans and Asians. APOE could cause ARF in the Europeans, but it was protective in the South Asians. Clinicians need to consider the characteristics of the local population before administering drugs to patients of different ethnicities.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors represent a novel approach for reducing cholesterol and, accordingly, the burden of atherosclerosis. However, limited data are available regarding the possible effects of PCSK9 inhibitors on atherosclerotic plaque. To evaluate the efficacy of PCSK9 inhibitors in reducing carotid plaque progression in individuals with high-risk carotid atherosclerotic disease. We used carotid total plaque area (TPA) to assess the burden of atherosclerosis. Ultrasound imaging of the carotid was acquired before and after the initiation of PCSK9 inhibitor therapy. We selected high-risk cases with atherosclerosis with a minimum of three ultrasound examinations, 1 year before, one at the time of initiation of a PCSK9 inhibitor, and 1 year after initiating a PCSK9 inhibitor. Statistical analysis was conducted using the mixed-effects model with Restricted Maximum Likelihood (REML). We reviewed data from 131 patients with a mean follow-up of 6 (±4) years. Patients were high-risk, with the majority having diabetes or hypertension. There was a decrease in TPA, particularly during the first 3 years after initiating PCSK9 inhibitor therapy (p < 0.05). Furthermore, we observed that individuals with higher baseline serum low-density lipoprotein cholesterol (LDL-C) levels experienced a greater decline in TPA (p < 0.05). PCSK9 inhibitors are effective in achieving plaque regression in high-risk patients with atherosclerosis. This is important, as plaque regression is associated with a lower risk of stroke, myocardial infarction, or vascular death.

The triglyceride-glucose index (TyG) and the triglyceride to high-density lipoprotein ratio (TG/HDL-c) are novel indicators for assessing insulin resistance (IR) in epidemiological studies. This study aimed to evaluate the association between 25-hydroxy-vitamin D [25(OH)D] levels and these two indicators in the adult population of the United States. 14,380 participants aged 20 years and older were included from the National Health and Nutrition Examination Survey (NHANES). Multivariable linear regression models were used to analyze the association between 25(OH)D and TyG, as well as TG/HDL-c. Smooth fitting curves were employed to identify potential non-linear relationships between 25(OH)D, TyG, and TG/HDL-c. The findings revealed a negative association between 25(OH)D and TyG, with the effect being more pronounced in males and individuals with diabetes (p < 0.01). Similarly, 25(OH)D was negatively associated with TG/HDL-c, with a stronger impact observed in males compared to females. The study population was divided into four quartiles based on 25(OH)D concentration, and TyG and TG/HDL-c levels in Q3 and Q4 were lower than those in Q1. Furthermore, a non-linear relationship was observed between 25(OH)D and TyG, with an inflection point at 19.352 ng/mL. A non-linear relationship was also found between TG/HDL-c and 25(OH)D, with an inflection point at 37.211 ng/mL. 25(OH)D is an independent factor significantly associated with TyG and TG/HDL-c indexes. This negative association may be related to the role of 25(OH)D in insulin resistance.

The order Rodentia comprises nearly 45% of all extant taxa, currently organized into 31 living families, some 450 genera, and roughly 2010 species (Kelt & Patton, 2020). Considering that rodents began evolving at least 66 million years ago, it is not surprising that they have diversified into five distinct suborders. With the advent of molecular biology, this difference can often be seen at the molecular level as well. Previous studies have indicated that the apolipoprotein E (APOE) of guinea pigs, belonging to the suborder Hystricomorpha, have fewer amino acids than have been reported for other suborders of Rodentia. Searching the genomic database for hystricomorph APOE genes, it was found that hystricomorphs were missing residues both in the vicinity of the hinge region and in the lipid-binding region of the apolipoprotein. In the hinge region, missing residues varied between 5 and 3, and in the latter region, seven residues were missing. The search also revealed that castorimorphs, although lacking the smaller of the two deletions, were also missing the same seven residue deletion as found in APOE of the hystricomorphs.

Non-communicable diseases (NCD) are associated with inflammation and oxidative stress which is further associated with omega-6 (ω6) and omega-3 (ω3) fatty acid (FA) imbalance favoring ω6 FA. By improving ω3 FA consumption, this imbalance can be altered to control NCD. Previously we have reported blends of flaxseed oil (FSO, ω3 FA) with palm olein (PO) or coconut oil (CO) were thermo-oxidatively stable with good storage stability and could improve ω6:ω3 ratio in cell lines. In the present study safety of these blends along with their efficacy to improve tissue FA composition particularly ω6:ω3 ratio was evaluated in Wistar rats. Institutional ethics committee approval was obtained initially. Wistar rats were supplemented with individual oils or blends (FSO with PO or CO, 20:80 by volume, 1.0 mL/day/200 gm body weight) for 3 months. Throughout the study period, there were no adverse effect of blends on feed intake and body weight gain. After 3 months, blood and serum were subjected for hematological, biochemical assessment. Vital organs were harvested for histopathological and FA composition investigations. Hematological, biochemical, and tissue histopathological parameters were comparable with Control (group receiving only normal diet). Interestingly serum lipid profile was improved by the blend supplementation. Except brain, FA composition was altered in liver, heart, adipose tissue, and RBC with lowering of ω6:ω3 ratio but there was no favorable effect on inflammatory markers and adipokines in the blend supplemented groups. Thus, to conclude, FSO blends with PO or CO were able to lower tissue ω6:ω3 ratio without adverse effects.

To examine the associations of apolipoprotein E (APOE) carrier status and lipid profiles with sleep disorders, including excessive daytime sleepiness (EDS) and probable rapid eye movement sleep behavior disorder (pRBD), among patients with early Parkinson's disease (PD) over 5-year follow-up periods. The Parkinson's Progression Markers Initiative is a multicenter cohort study based on an ongoing and open-ended registry. Data from baseline and 5-year follow-up visits from participants of de novo PD were analyzed. Longitudinal associations of APOE carrier status and lipid profiles with sleep disorders were estimated via linear mixed-effects models. A total of 657 participants with complete APOE genotypes were enrolled at baseline. Among them, 153 (25.3%) had available lipid profiles at baseline. In the linear mixed-effects models, baseline APOE ε2/ε3/ε4 carrier status did not exhibit significant associations with EDS and pRBD (all p > 0.05) in all models. However, reduced high-density lipoprotein (HDL) and elevated triglycerides (TG) were associated with developing EDS (β = −0.04, 95% CI: −0.07, −0.00) and pRBD (β = 0.01, 95% CI: 0.00, 0.02) in PD patients, respectively. In the APOE ε4+ subgroup, decreased HDL and increased TG displayed substantial associations with developing EDS and sleep disorders (all p < 0.05) in all models, respectively, whereas no significant differences were noted in the APOE ε4− subgroup (all p > 0.05). Our study did not demonstrate a clear association between APOE ε2/ε3/ε4 and sleep disorders in PD patients. However, the presence of APOE ε4 was associated with changes in lipid profiles, notably affecting TG and HDL levels.