High cholesterol absorption efficiency is determined by genetic variation in small intestinal sterol transporters and affects one-third of individuals. Their risk for atherosclerotic cardiovascular disease (ASCVD) is increased compared with low cholesterol absorbers, despite similar serum lipid concentrations. We investigated the association of cholesterol absorption efficiency with proatherogenic properties of low-density lipoproteins (LDLs). The study cohort consisted of 90 middle-aged participants, 56 females and 34 males, without lipid-lowering therapy or ASCVD. They were divided into low (n=45) and high (n=45) cholesterol absorbers by the median value of serum cholestanol to cholesterol ratio. LDL aggregation susceptibility and binding of lipoproteins to proteoglycans were determined as biomarkers of lipoprotein atherogenicity. Nuclear magnetic resonance spectroscopy, mass spectrometry, and gas-liquid chromatography were used to determine lipoprotein subclass profile, LDL lipidome, and serum concentrations of cholesterol and noncholesterol sterols, respectively. Age, dietary cholesterol, and serum total cholesterol or lipoprotein cholesterol levels did not differ between the groups. In the high absorbers, LDL particles were larger, and LDL aggregation susceptibility and the binding of lipoproteins to proteoglycans were increased in the low absorbers. Of LDL surface lipids, sphingomyelin 42:3;O2, and phosphatidylcholine (PC) 32:0 correlated positively, whereas PC 32:1 correlated negatively with serum cholestanol levels. These LDL surface lipids were also associated with increased LDL aggregation susceptibility and proteoglycan-binding. The present findings suggest that increased proatherogenic properties in high cholesterol absorbers may contribute to increased ASCVD risk. https://clinicaltrials.gov/study/NCT01315964.

Amyotrophic lateral sclerosis (ALS) is a heterogeneous neurodegenerative disorder. Notably, the differences in lipid metabolism between bulbar- and limb-onset subtypes of ALS remain unclear, particularly in non-Western populations. The present study investigated serum lipid profiles in a Chinese cohort of patients with ALS to explore their associations with disease severity and clinical subtypes. A retrospective, cross-sectional study was conducted, involving 158 patients with ALS and 62 matched healthy controls. Serum lipid parameters, including total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), small dense LDL cholesterol (sdLDL-c), apolipoprotein A-1 (ApoA1), apolipoprotein B (ApoB) and the TG/HDL ratio, were compared between the groups. Correlation analyses and multivariable linear regression models incorporating phenotype x lipid interaction terms were conducted after adjusting for age, sex, body mass index and disease duration. Patients with ALS exhibited significantly higher TC, TG, LDL, sdLDL-c, ApoA1, ApoB and TG/HDL ratios than controls. Subtype-specific analyses revealed different associations; in bulbar-onset ALS, higher sdLDL-c and TG/HDL ratios were associated with better functional status, whereas higher HDL and ApoA1 levels were negatively correlated with functional status. By contrast, in limb-onset ALS, higher sdLDL-c and ApoB levels were associated with worse function. Interaction analyses confirmed significant phenotype modification for sdLDL-c, TG/HDL ratio, HDL and ApoA1. These results suggest that lipid-severity relationships in ALS vary by subtype, indicating metabolic heterogeneity across phenotypes and supporting the potential of specific lipid parameters as exploratory markers for disease monitoring.

A dual-signal electrochemical aptasensor based on rGO@MoS2-Fc nanozyme for sensitive detection of low-density lipoprotein.

Hypocholesterolemia is a consequence, not a cause, of kidney cancer: A bidirectional Mendelian randomization study with NHANES 2001-2018.

Cardiovascular disease (CVD) is the predominant cause of morbidity and mortality among patients with type 1 or type 2 diabetes. The association between hyperglycemia and intracellular metabolic changes can result in oxidative stress, low-grade inflammation, and endothelial dysfunction. The management of hyperglycemia and prediabetes-associated vascular complications rely on pharmacotherapy and lifestyle intervention strategies. Research investigated the cardio-protective effects of Momordica balsamina in a diet-induced prediabetic rats. Prediabetes was induced using a laboratory established protocol in male Sprague Dawley rats. Thereafter, M. balsamina (250 mg/kg) was administered to prediabetic rats once a day every third day in the presence or absence of dietary intervention. Blood pressure and plasma glucose concentration were monitored throughout the study. Blood and tissue were collected for biochemical analysis. M. balsamina with or without dietary intervention resulted into a reduction in mean arterial blood pressure. In addition, there was a significant decrease in the heart tissue malondialdehyde and increased plasma superoxide dismutase and glutathione peroxidase concentration. Furthermore, there was a decrease in plasma triglycerides, low-density lipoprotein with an increased high-density lipoprotein concentration Lastly, M. balsamina with or without dietary intervention demonstrated a reduced plasma tumor necrosis factor alpha and reduced interleukin-6 concentrations in the absence of dietary intervention. M. balsamina coupled with or without dietary intervention decreased the risk of developing cardiac injury, thus preventing cardiovascular disease in prediabetes. Therefore, this medicinal plant may be a beneficial therapeutic agent in the prevention of prediabetic cardiovascular complications.

Foods rich in anti-inflammatory components and anti-inflammatory supplements for the prevention and treatment of Sarcopenia in older adults: A systematic review and network meta-analysis.

The aim of this study was to investigate the effects of a moderate-intensity multicomponent training (MCT) program on body composition, physical function, glycaemic control and lipid profiles in overweight and obese older people. This single-arm quasi-experimental study included 48 male (n = 10) and female (n = 38) overweight (n = 27) and obese (n = 21) older individuals (69.2 ± 4.3 years; 76.4 ± 12.3 kg; 1.60 ± 0.1 m; 30.3 ± 4.7 kg·m2) who were subjected to a 36-week moderate-intensity MCT intervention, including strength, stretching, endurance and balance exercises, twice a week, along with nutritional counselling and psychoeducation. Body composition, physical function (upper- and lower-body strength endurance, lower-body flexibility and dynamic balance), fasting plasma glucose, total cholesterol (TC), low-density lipoprotein (LDL-c) and high-density lipoprotein (HDL-c) levels were assessed before and after 12, 24 and 36 weeks of intervention. Food consumption was evaluated at baseline and after 36 weeks. Except for TC (p = 0.58; W = 0.014), a significant improvement was detected in LDL-c (p < 0.001; W = 0.132) and HDL-c (p < 0.001; W = 0.195), as well as in fasting glucose (p < 0.001; W = 0.556). Upper- and lower-body strength endurance (both p < 0.0001, W = 0.447 and W = 0.175, respectively), lower-body flexibility (p = 0.02; W = 0.068) and dynamic balance (p = 0.04; W = 0.060) also improved in response to MCT. However, all body composition outcomes remained unchanged throughout the MCT intervention (all p > 0.05). Similarly, no significant differences were identified in the food intake variables (all p > 0.05). Our moderate-intensity MCT program effectively improved physical function, glycaemic control and lipid profile, but not body composition, in overweight and obese older adults.

Quadriceps fat pad impingement: where patellofemoral maltracking meets the metabolic-inflammatory axis.

Neuropeptide analog PD149163 ameliorates metabolic endotoxemia-driven thyroid inflammation by targeting LPS-LBP signalling in murine model: Insights from in vivo, in silico and network pharmacology analyses.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD). Currently, no approved targeted therapeutic interventions exist for MASLD. Hypoxia is known to exacerbate the progression of both MASLD and ASCVD. Notably, peroxisome proliferator-activated receptor α (PPARα), a key regulator of lipid metabolism, has also been implicated in modulating cellular adaptation to hypoxic conditions. This study aims to elucidate the role of PPARα in arterial endothelial cell dysfunction by investigating its involvement in lipid metabolism reprogramming within the context of MASLD under high-altitude hypoxia. We observed that chronic hypoxia exacerbates the increase in low-density lipoprotein (LDL) levels and elevates the risk of ASCVD in MASLD patients. In MASLD mice, chronic hypoxia activates hepatic hypoxia-inducible factor 2-alpha (HIF-2α), which suppresses PPARα, leading to decreased expression of low-density lipoprotein receptor (LDLR) and ATP-binding cassette subfamily G member 8 (ABCG8), consequently raising serum LDL levels and indirectly reducing endothelial nitric oxide synthase (eNOS) expression in arterial endothelial cells. Activation of PPARα can upregulate the expression of LDLR and ABCG8 in hepatocytes, thereby improving fatty liver and restoring the function of aortic endothelial cells. Our study identifies chronic hypoxia induces liver HIF-2α, which inhibits PPARα and impairs hepatic cholesterol metabolism. This leads to MASLD progression and increased ASCVD risk, as impaired cholesterol metabolism negatively affects endothelial cell function. Activation of PPARα enhances hepatic lipid metabolism, thereby indirectly improving endothelial cell function. Moreover, we demonstrate that fenofibrate represents a viable and cost-effective therapeutic strategy for ameliorating MASLD and preventing ASCVD under hypoxic conditions.

Elevated concentrations of both low-density lipoprotein (LDL)-cholesterol and lipoprotein(a) [Lp(a)] is probably the most detrimental lipid profile in terms of cardiovascular health. Our primary objective was to review the reports published before January 2026 pertaining to the metabolism of lipoprotein(a) and associated cardiovascular disease (CVD) risk specifically in familial hypercholesterolemia. Lp(a) has consistently been found elevated in familial hypercholesterolemia (FH) cohorts. To a large extent, this results from the fact that elevated Lp(a) increases the likelihood for a patient to be clinically diagnosed as FH. For long, increases in Lp(a) concentrations observed in FH patients have been regarded as the consequence of impaired Lp(a) plasma clearance by the LDL receptor. However, recent studies strongly advocate against a significant role for the LDL receptor in mediating Lp(a) hepatic uptake. The molecular mechanisms by which Lp(a) is cleared from blood still remain elusive. Finally, mounting clinical evidence indicates that lowering LDL-C pharmacologically will not offset the specific cardiovascular risk stemming from elevated Lp(a) in FH. It is highly recommended to systematically measure Lp(a) in FH patients. These patients should be treated with high-dose statins, when necessary, in combination with a proprotein convertase subtilisin/kexin type 9 inhibitor to reach LDL-C therapeutic goals. Hopefully, the Lp(a) lowering therapies currently under development will prove instrumental for adequate treatment of FH patients with concomitantly elevated Lp(a) in coming years.

Prediction of early neurological deterioration using quantitative susceptibility mapping in small artery occlusion ischemic stroke.

Dietary Aspergillus niger filtrate: A natural supplement to boost quail breeder productivity and health.

Sigma-2 receptor modulators alter low-density lipoprotein receptor-mediated lipid uptake in retinal pigment epithelial cells.

Cyclodextrin metal-organic framework engineered titanium surface: Targeted modulation of foam cell lipid homeostasis and inflammatory resolution.

Dietary intervention modifies low-density lipoproteins particle size according to genetic variability: a clinical study.

Therapeutic potential of Olea europaea leaf extract in preventing isoproterenol-induced myocardial injury: integrated biochemical, LC-MS profiling, and molecular docking analyses.

Hibernation is an amazing survival skill that some animals use to cope with natural challenges, and cold is the main stimulus. While most hibernation studies focus on long-term cold adaptation mechanisms, the rapid physiological adjustments triggered by short-term cold exposure may also be key components in the initiation of hibernation. This study focused on 20 Chinese Moccasin (Deinagkistrodon acutus), divided into two groups: an active group (n = 10) and a short-term cold exposure group (n = 10). Using serum biochemistry, serum antioxidant measurements, and liver transcriptome technology, the study explored the effects of short-term cold exposure on snake serum lipids, antioxidant capacity, and apoptosis. The results showed that the levels of cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol were significantly lower in cold exposure snakes compared to the active group, whereas total bile acid was higher in the cold exposure group; serum antioxidant indicators glutathione peroxidase, superoxide dismutase, and total antioxidant capacity were lower in cold exposure snakes than in active snakes, whereas the concentration of malondialdehyde was higher in cold exposure snakes. The liver transcriptome revealed that more pro-apoptotic genes were upregulated in active snakes, whereas there were more upregulated anti-apoptotic genes in cold exposure snakes, and the ratio of anti-apoptotic to pro-apoptotic genes was significantly higher in cold exposure snakes than in active snakes. This study not only elucidates the physiological effects of short-term cold exposure on snakes but also advances our understanding of the adaptive mechanisms underlying the transition from activity to hibernation in ectothermic animals.

Patients with schizophrenia spectrum disorders (SSDs) have a higher risk for post-diagnostic cardiometabolic comorbidities. While antipsychotic use partly explains this, the contribution of genetic susceptibility remains unclear. We investigated the relationships between cardiometabolic-related polygenic risk scores (PRSes) with cardiometabolic outcomes using data from 671 patients with SSDs in the Dutch Genetic Risk and Outcome of Psychosis study. Seven PRSes were calculated for body mass index (BMI), high- and low-density lipoprotein cholesterol (HDL, LDL), triglycerides, glucose, systolic (SBP) and diastolic blood pressure (DBP) using summary statistics from most recent genome-wide association studies. Four linear regression models assessed the cross-sectional associations between PRSes and cardiometabolic outcomes including BMI, HDL, LDL, triglycerides, glycated hemoglobin, SBP, DBP, and a composite metabolic score. Model #1 included baseline factors (age, sex, and population substructure); #2 included model 1 with a single-trait PRS; #3 included model 1 with all PRSes of designated traits; and #4 included model 1 and a composite PRS score. All seven cardiometabolic PRSes were significantly associated with their corresponding outcomes. Significant cross-trait associations were observed including PRSBMI with lower HDL (explained variance (R2)=2.33%), higher DBP (R2=3.35%), and higher SBP (R2=2.29%); PRSHDL with higher HDL(R2=2.05%) and LDL levels(R2=2.31%); PRSDBP with higher SBP(R2=1.75%), and PRSSBP with higher DBP(R2=2.94%). The current study suggests that genetic susceptibility contributes modestly but significantly to poor cardiometabolic outcomes. Shared genetic susceptibility may underpin the frequent co-occurrence of cardiometabolic morbidities in SSDs, supporting the potential utility of PRSes in identifying high-risk patients for early intervention in practice.

Fluorine is a trace element that is beneficial to human health. However, long-term and excessive fluoride exposure can damage bone and teeth, as well as the cardiovascular, nervous, and reproductive systems, etc. Since 2001, a growing body of evidences suggests that excessive fluoride exposure is associated with cardiovascular diseases. Although some original studies have focused on this topic, general and narrative reviews are rare. This article summarizes the effects of fluoride on blood pressure/hypertension, vascular sclerosis (mainly atherosclerosis), and myocardial/ cardiac damages based on epidemiologic investigations, in vivo and in vitro mechanistic studies. Most studies suggest that excessive fluoride exposure can initiate and aggravate hypertension through endothelial dysfunction (ED) manifested as abnormal endothelium metabolism, endothelium apoptosis, hyper-permeability, and impaired vasomotor function (imbalance of endothelin-1/nitric oxide), oxidative stress (over generation of ROS), and abnormal activities of the renin-angiotensin-aldosterone system covered up-regulation of AT1R, AT2R, ACE3 and down-regulation of ACE2. Besides ED, excessive fluoride exposure induced and accelerated atherosclerosis via lipid metabolism disorders (elevated plasma triglyceride, total cholesterol, and low-density lipoprotein cholesterol, etc. levels), up-regulation of adhesion molecules (P-selectin, ICAM-1 and VCAM-1), over-proliferation and phenotypic changes of vascular smooth muscle cells. Except for oxidative stress, excessive fluoride exposure caused myocardial and cardiac functional damage via myocardium injuries, inflammation (IL-6 and IL-10 increased), and mitochondrial dysfunction (ATP and ATPase decreased), then presenting electrocardiographic abnormalities. The review will help to clarify harms of fluoride on the cardiovascular system and provide basis for adjustments of drinking water standards.