Lipids最新文献

Accurate estimation of low-density lipoprotein cholesterol (LDL-C) is important for monitoring cardiovascular disease (CVD) risk and guiding lipid-lowering therapy. This study aimed to evaluate the magnitude of discordance of LDL-C levels calculated by different equations and its effect on CVD incidence. The study sample consisted of 2354 CVD-free individuals (49% males, mean age 45 ± 14 years); 1600 were re-evaluated at 10 years and 1570 at 20 years. LDL-C was estimated using the Friedewald, Martin/Hopkins, and Sampson equations. Participants were categorized as discordant if estimated LDL-C was below the CVD-risk specific cut-off for one equation and equal/above for its comparator. The Friedewald and Martin/Hopkins equations presented a similar performance in estimating LDL-C; however, both yielded lower values compared to the Sampson. In all pairwise comparisons, differences were more pronounced at lower LDL-C levels, while the Friedewald equation significantly underestimated LDL-C in hypertriglyceridemic participants. Discordance was evident in 11% of the study population, and more specifically 6%, 22%, and 20% for Friedewald versus Martin/Hopkins, Friedewald versus Sampson and Martin/Hopkins versus Sampson equations, respectively. Among discordant participants, median (1st, 3rd quartile) difference in LDL-C was −4.35 (−10.1, 1.95), −10.6 (−12.3, −9.53) and −11.3 (−11.9, −10.6) mg/dL for Friedewald versus Martin/Hopkins, Friedewald versus Sampson and Martin/Hopkins versus Sampson equations, respectively. The 10- and 20-year CVD survival model that included LDL-C values of the Martin-Hopkins equation outperformed the predictive ability of those based on the Friedewald or Sampson equations. Significant differences in estimated LDL-C exist among equations, which may result in LDL-C underestimation and undertreatment.

Enrichment of egg yolks with very long chain omega-3 fatty acids (VLCn-3 FA) is of interest because of their beneficial effects on human health. The ability of Ahiflower® oil (AHI; Buglossoides arvensis), which is naturally rich in stearidonic acid (SDA), and a high-alpha-linolenic acid (ALA) flaxseed (FLAX) oil to enrich eggs and tissues of laying hens with VLCn-3 FA was investigated. Forty 54-week-old Hy-Line W-36 White Leghorn hens were fed a diet that contained soybean oil (control; CON) or AHI or FLAX oils at 7.5 or 22.5 g/kg of the diet in substitution for the soybean oil for 28 days. Dietary treatments had no effects on egg number or components or follicle development. Total VLCn-3 FA contents of egg yolk, liver, breast, thigh, and adipose tissue were greater in the n-3 treatments compared to CON, with the greatest increase observed at the higher oil level, especially for AHI oil which had the greater VLCn-3 enrichment than FLAX in yolk (p < 0.001). Efficiency of VLCn-3 enrichment of egg yolks was decreased with n-3 oils and by increasing oil level with lowest efficiency at 22.5 g/kg FLAX. In conclusion, both SDA-rich (AHI) and ALA-rich (FLAX) oils increased VLCn-3 FA deposition into egg yolks and hens' tissues, but dietary AHI oil promoted a greater enrichment than comparative amounts of FLAX oil, especially in liver and egg yolks.

The bioavailability of long-chain omega-3 polyunsaturated fatty acids (n3 PUFA) can be affected by the form in which they are bound. An alternative source of n3 PUFA is Calanus finmarchicus oil (CO), which, unlike fish oil (FO) and krill oil (KO), contains fatty acids primarily bound as wax esters. Recent studies have shown that n3 PUFA from CO are bioavailable to humans, but CO has not been compared to other marine oils such as FO or KO. Therefore, the aim of this study was to investigate the influence of 12 weeks supplementation with CO, FO and KO on the long-term n3 PUFA status in healthy volunteers. The Omega-3 Index (O3I), defined as red blood cell EPA + DHA content as a percentage of total identified fatty acids, was used as a measure to assess n3 PUFA status. Sixty-two participants (mean ± standard deviation [SD] age: 29.7 ± 8.43 years) completed the randomized parallel group study (CO group: n = 21, 4 capsules/day, EPA + DHA dose: 242 mg/day; FO group: n = 22, 1 capsule/day, EPA + DHA dose: 248 mg/day; KO group: n = 19, 2 capsules/day, EPA + DHA dose: 286 mg/day). At baseline, the three groups showed comparable (mean ± SD) O3I values (CO: 5.13 ± 1.12%, FO: 4.90 ± 0.57%, KO: 4.87 ± 0.77%). The post-interventional (mean ± SD) O3I increase was comparable between the three groups (CO: 1.09 ± 0.55%; FO: 1.0 ± 0.53%; KO: 1.15 ± 0.65%, all p < 0.001). The study confirms that CO can increase the n3 PUFA status comparable to FO and KO and is therefore an alternative marine source of bioavailable n3 PUFA, especially with regard to sustainability.

This study aimed to investigate the effect of fatty acid-ethanol amine (FA-EA) derivatives (L1–L10) on the mitigation of intracellular lipid accumulation and downregulation of pro-inflammatory cytokines in vitro. First, the series of FA-EA derivatives were synthesized and characterized. Then, their cytotoxic, intracellular lipid accumulation and inhibition of pro-inflammatory cytokines were evaluated. The oil red O staining experiment showed that the tested compounds L4, L6, L8, L9, and L10 could reduce intracellular lipid accumulation induced by palmitic acid (PA). Moreover, ω-3/ω-6 PUFA-EA derivatives showed inhibitory effect on the production of pro-inflammatory cytokines in lipopolysaccharide (LPS) -stimulated RAW 264.7 cells. ω-3/ω-6 PUFA-EA derivatives at a concentrations of 10 μM could significantly decrease mRNA levels of IL-6, IL-1β, and TNF-α, inhibit NO production, and alleviate the protein expression of IL-1β in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. These data suggest that ω-3 PUFA-EA derivatives can be beneficial for further pharmaceutical development to treat chronic low-grade inflammation diseases such as obesity.

We investigated the relationships between ceramide species concentrations in liver, plasma and very low-density lipoproteins (VLDL) particles of humans with obesity as well as the relationships between hepatic fat content and hepatic ceramide concentrations and proportional distribution. Twenty-five obese (body mass index >35 kg/m²) adults participated in this study. Plasma, VLDL and hepatocellular ceramide concentrations were measured by liquid chromatography/tandem mass spectrometry. The proportionate distribution of measured ceramide species differed between liver, whole plasma and the VLDL fraction. We found significant, positive correlations between the proportion of C14:0, C18:0, C20:0 and C24:1 ceramide in the liver and whole plasma (γ = 0.491, p = 0.013; γ = 0.573, p = 0.003; γ = 0.479, p = 0.015; γ = 0.716, p = 0.00006; respectively). In contrast, only the proportional contribution of C24:1 ceramide correlated positively between VLDL and liver (γ = 0.425, p = 0.013). The percent hepatic fat correlated positively with the proportion of C18:1, C18:0 and C20:0 hepatic ceramides (γ = 0.415, p = 0.039; γ = 0.426, p = 0.034; γ = 0.612, p = 0.001; respectively), but not with total hepatic ceramide concentration. The proportions of whole plasma ceramide subspecies, especially C14:0, C18:0, C20:0 and C24:1chain length, are reflective of those of hepatic ceramide subspecies in obese humans; these appear to be markers of hepatic ceramide species composition.

Cancer cells are known to survive in a hypoxic microenvironment by altering their lipid metabolism as well as their energy metabolism. In this study, Caco-2 cells derived from human colon cancer, were found to have elevated intracellular levels of phosphatidic acid and its lysoform, lysophosphatidic acid (LPA), under hypoxic conditions. Our results suggested that the elevation of LPA in Caco-2 cells was mainly due to the combined increases in cellular levels of lysophosphatidylcholine and lysophosphatidylethanolamine by phospholipase A₂ and subsequent hydrolysis to LPA by lysophospholipase D. We detected the Ca²⁺-stimulated choline-producing activities toward exogenous lysophosphatidylcholines in whole Caco-2 cell homogenates, indicating their involvement in the LPA production in intact Caco-2 cells.

Leishmania parasites are the causative agents of visceral or cutaneous leishmaniasis in humans and of canine leishmaniosis. The macrophage is the predilected host cell of Leishmania in which the promastigote stage is transformed into amastigote. We previously showed changes in the fatty acid composition (FA) of lipids in two strains of Leishmania donovani upon differentiation of promastigote to amastigote, including increased proportions of arachidonic acid (AA) and to a less extent of docosahexaenoic acid (DHA). Here, we carried out supplementation with AA or DHA on two Leishmania infantum strains, a visceral (MON-1) and a cutaneous (MON-24), to evaluate the role of these FA in parasite/macrophage interactions. The proportions of AA or DHA in total lipids were significantly increased in promastigotes cultured in AA- or DHA-supplemented media compared to controls. The content of FA-derived oxygenated metabolites was enhanced in supplemented strains, generating especially epoxyeicosatrienoic acids (11,12- and 14,15-EET) and hydroxyeicosatetraenoic acids (5- and 8- HETE) from AA, and hydroxydocosahexaenoic acids (14- and 17-HDoHE) from DHA. For both MON-1 and MON-24, AA-supplemented promastigotes showed higher infectivity towards J774 macrophages as evidenced by higher intracellular amastigote numbers. Higher infectivity was observed after DHA supplementation for MON-24 but not MON-1 strain. ROS production by macrophages increased upon parasite infection, but only minor change was observed between control and supplemented parasites. We propose that under high AA or DHA environment that is associated with AA or DHA enrichment of promastigote lipids, FA derivatives can accumulate in the parasite, thereby modulating parasite infectivity towards host macrophages.

Furan fatty acids (FuFA) are important antioxidants found in low concentrations in many types of food. In addition to conventional FuFA which normally feature saturated carboxyalkyl and alkyl chains, a few previous studies indicated the FuFA co-occurrence of low shares of unsaturated furan fatty acids (uFuFA). For their detailed analysis, the potential uFuFA were enriched by centrifugal partition chromatography (CPC) or countercurrent chromatography (CCC) followed by silver ion chromatography from a 4,7,10,13,16,19-docosahexaenoic acid ethyl ester oil, a 5,8,11,14,17-eicosapentaenoic acid ethyl ester oil and a latex glove extract. Subsequent gas chromatography with mass spectrometry (GC/MS) analysis enabled the detection of 16 individual uFuFA isomers with a double bond in conjugation with the central furan moiety. In either case, four instead of two uFuFA isomers previously reported in food, respectively, were detected by GC/MS. These isomers showed characteristic elution and abundance patterns in GC/MS chromatograms which indicated the presence of two pairs of cis/trans-isomers (geometrical isomers).

Olive oil has beneficial effects on skin wound healing due to its anti-inflammatory and antioxidant properties; however, the mechanism by which olive oil promotes wound healing is unclear. We evaluated the mechanisms involved in Nrf2 pathway activation by olive oil and its role in cell survival and migration in mouse dermal fibroblasts in a short-term exposition. Our data demonstrated that olive oil and oleic acid promoted reactive oxygen species (ROS) production, while olive oil and hydroxytyrosol stimulated nuclear factor erythroid 2-related factor 2 (Nrf2) activation. Olive oil-mediated ROS production increased nuclear factor kappa B p65 expression, while olive oil-stimulated reactive nitrogen species production augmented the levels of Nrf2. Olive oil augmented cell proliferation, cell migration, and AKT phosphorylation, but decreased apoptotic cell number and cleaved caspase-3 levels. The effect of olive oil on cell migration and protein levels of AKT, BCL-2, and Nrf2 were reversed by an Nrf2 inhibitor. In conclusion, the activation of the Nrf2 pathway by olive oil promotes the survival and migration of dermal fibroblasts that are essential for the resolution of skin wound healing.

Omega-3 polyunsaturated fatty acids (omega-3 PUFAs) are essential for improving the health and performance of athletes. The present study aimed to evaluate the nutritional status of omega-3 PUFAs in Chinese elite athletes by both dietary intake analysis and serum biomarker detection. A cross-sectional analysis of data from 54 elite athletes (24 men and 30 women) from Shanghai professional sports teams was conducted. A food frequency questionnaire (FFQ) was employed to analyze dietary intake, and gas chromatography–mass spectrometry (GC–MS/MS) was conducted to measure serum biomarkers of PUFAs. Correlation analysis was performed to investigate the relationships of PUFA biomarkers with diet, inflammation and oxidative stress. The results showed that the median intake of EPA + DHA among athletes was 132 mg/d, which is lower than the minimum value recommended by dietary guidelines (250 mg/d). The average serum EPA + DHA was 4.0 ± 1.1%, and the ratio of omega-6/omega-3 was 7.7 ± 1.7. Most (96.3%) of the athletes were below the targeted value of serum EPA + DHA, which is associated with a reduction in cardiovascular risk. Correlation analysis showed that the serum EPA + DHA was positively correlated with the long-term dietary intake of EPA + DHA and negatively correlated with inflammatory markers. In conclusion, the serum circulating EPA + DHA and omega-6/omega-3 ratio are effective biomarkers reflecting the nutritional status of PUFAs in athletes. Omega-3 PUFAs have a potential effect on inhibiting inflammatory markers. Hence, it is necessary for Chinese athletes to improve their suboptimal nutritional status of PUFAs through dietary intervention.