Lipids最新文献

Hydrophilic endogenous bile acids ursodeoxycholic acid (UDCA), tauroursodeoxycholic acid (TUDCA), and glucourosodeoxycholic acid (GUDCA) have suggested neuroprotective effects. We performed a case–control study to examine the association between ALS diagnosis and serum levels of bile acids. Sporadic and familial ALS patients, age- and sex-matched healthy controls, and presymptomatic gene carriers who donated blood samples were included. Non-fasted serum samples stored at −80°C were used for the analysis. Serum bile acid levels were measured by liquid chromatography-mass spectrometry (LC–MS). Concentrations of 15 bile acids were obtained, 5 non-conjugated and 10 conjugated, and compared between ALS versus control groups (presymptomatic gene carriers + healthy controls) using the Wilcoxon-Rank-Sum test. In total, 80 participants were included: 31 ALS (17 sporadic and 14 familial ALS); 49 controls (22 gene carriers, 27 healthy controls). The mean age was 50 years old and 50% were male. In the ALS group, 45% had familial disease with a pathogenic variant in C9orf72 (29%), TARDBP (10%), FUS (3%), and CHCHD10 (3%) genes. In the control group, 43% carried pathogenic variants: C9orf72 (27%), SOD1 (10%), and FUS (6%). The serum levels of UDCA, TUDCA, and GUDCA trended higher in the ALS group compared to controls (median 27 vs. 7 nM, 4 vs. 3 nM, 110 vs. 47 nM, p-values 0.04, 0.06, 0.04, respectively). No significant group differences were found in other bile acids serum levels. In conclusion, the serum level of UDCA, TUDCA, GUDCA trended higher in ALS patients compared to controls, and no evidence of deficiencies was found.

Type 2 diabetes mellitus (T2DM) is a highly prevalent metabolic disorder. Insulin resistance and oxidative stress are associated with T2DM development. The hypothesis that patients with T2DM show excess accumulation of lipids, such as ceramides (Cers) and diacylglycerols (DAGs), in their skeletal muscles has been widely supported; however, detailed lipidomic data at the molecular species level are limited. Therefore, in this study, we aimed to investigate the in vitro dynamics of total lipids, including phospholipids (PLs), sphingolipids, and neutral lipids, in palmitic acid-induced insulin-resistant C2C12 skeletal muscle cells. Our data demonstrated that the profiles of not only Cers and DAGs but also those of PLs showed considerably differences after palmitate treatment. We found that PL synthesis reduced and PL degradation increased after palmitate treatment. These findings may aid in the development of treatments to ameliorate muscle dysfunction caused by lipid accumulation in muscles.

High-fat diets have been associated with colorectal cancer (CRC) risk, and the role of polyunsaturated fatty acids (PUFAs) has been reported to vary based on the length of PUFAs. We explored the association between dietary omega-6 and omega-3 PUFAs intake and CRC. We analyzed 865 CRC patients and 3206 controls from a case–control study of Iran (IROPICAN study). We used multivariate logistic regression models to calculate the odds ratios (OR) and 95% confidence intervals (CI) for the association between PUFAs intake and CRC risk. Our results showed that gamma-linolenic acid (18:3 n-6, GLA), arachidonic acid (20:4n-6, ARA), a-linolenic acid (Cis-18:3n-3, ALA), eicosapentaenoic acid (20:5n-3, EPA), docosahexaenoic acid (22:6n-3, DHA) consumption was not associated with the risk of CRC. However, the OR of linoleic acid (18: 2n-6, LA) intake was 1.47 (95% CI 1.01–2.14, p = 0.04) for proximal colon and that of docosapentaenoic acid (22:5n-3, DPA) intake was 1.33 (95% CI 1.05–1.69, p = 0.01) for rectum. This study indicates a high level of LA is associated with an increased risk of proximal colon cancer, and DPA intake was positively associated with rectum cancer risk. Furthermore, our study noted a high intake of n-6 (from vegetable oils) compared to n-3 PUFAs (from fish and seafood) in this population. Public awareness and government support is needed to increase fish and seafood production and consumption in Iran.

Recent studies have identified monocyte-to-high-density lipoprotein cholesterol ratio (MHR) as a simple marker of atherosclerosis. Abdominal aortic calcification (AAC) is a direct result of vascular atherosclerosis. Our study aims to investigate the association between MHR and the prevalent extensive AAC and assess the value of MHR for identifying prevalent extensive AAC. 2857 subjects (28.07%) from the cross-sectional National Health and Nutrition Examination Survey 2013–2014 were included in our study. AAC was detected through dual-energy x-ray absorptiometry and quantified by Kauppila score. Extensive AAC was identified in 153 (10.44% of 1465) females and 146 (10.49% of 1392) males. With the full adjustment, each SD increase of MHR resulted in an 87.3% additional risk for extensive AAC in females. When dividing into quartiles, the top quartile had a 3.472 times risk of prevalent extensive AAC than the bottom quartile. However, no significant association was observed in males. Furthermore, smooth curve fitting implicated that the significant association was linear in the whole range of MHR among females. Additionally, ROC demonstrated an improvement in the identification of extensive AAC only among females when introducing MHR into established risk factors of atherosclerosis (0.808 vs. 0.864, p < 0.001). Finally, category-free net reclassification index and integrated discrimination index also supported the improvement by MHR in females. Our study revealed a linear association between MHR and prevalent extensive AAC in females. Moreover, our results implicated the potential value of MHR to refine the identification of prevalent extensive AAC in females.

The low-protein, high-carbohydrate (LPHC) diet administered to growing rats soon after weaning, for 15 days, promoted an increase in energy expenditure by uncoupling protein 1 (UCP1) in interscapular brown adipose tissue, and also due to the occurrence of the browning process in the perirenal white adipose tissue (periWAT). However, we believe that inguinal white adipose tissue (ingWAT) may also contribute to energy expenditure through other mechanisms. Therefore, the aim of this work is to investigate the presence of the futile creatine cycle, and the origin of lipids in ingWAT, since that tissue showed an increase in the lipids content in rats submitted to the LPHC diet for 15 days. We observed increases in creatine kinase and alkaline phosphatase activity in ingWAT, of the LPHC animals. The mitochondrial Nicotinamide adenine dinucleotide reduced/nicotinamide adenine dinucleotide oxidized ratio is lower in ingWAT of LPHC animals. In the LPHC animals treated with β-guanidinopropionic acid, the extracellular uptake of creatine in ingWAT was lower, as was the rectal temperature. Regarding lipid metabolism, we observed that in ingWAT, lipolysis in vitro when stimulated with noradrenaline is lower, and there were no changes in baseline levels. In addition, increases in the activity of enzymes were also observed: malic, glucose-6-phosphate dehydrogenase, and ATP-citrate lyase, in addition to an increase in the PPARγ content. The results show the occurrence of the futile creatine cycle in ingWAT, and that the increase in the relative mass may be due to an increase in de novo fatty acid synthesis.

The linoleic acid (LA)-arachidonic acid (ARA)-inflammatory axis suggests dietary LA lowering benefits health because it lowers ARA and ARA-derived endocannabinoids (ECB). Dietary LA reduction increases concentrations of omega-3 eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and DHA derived ECB. The aim of this study was to examine targeted reduction of dietary LA, with and without EPA and DHA, on plasma EPA and DHA and ECB (2-arachidonoyl glycerol [2-AG], anandamide [AEA], and docosahexaenoyl ethanolamide [DHA-EA]). Healthy, pre-menopausal women (n = 62, BMI 30 ± 3 kg/m², age 35 ± 7 years; mean ± SD) were randomized to three 12-week controlled diets: (1) high LA, low omega-3 EPA and DHA (H6L3); (2) low LA, low omega-3 EPA and DHA (L6L3); or (3) low LA, high omega-3 EPA and DHA (L6H3). Baseline plasma fatty acids and ECB were similar between diets. Starting at 4 weeks, L6L3 and L6H3 lowered plasma LA compared to H6L3 (p < 0.001). While plasma ARA changed from baseline by 8% in L6L3 and −8% in L6H3, there were no group differences. After 4 weeks, plasma EPA and DHA increased from baseline in women on the L6H3 diet (ps < 0.001) and were different than the H6L3 and L6L3 diets. No differences were found between diets for AEA or 2-AG, however, in L6L3 and L6H3, AEA increased by 14% (ps < 0.02). L6H3 resulted in 35% higher DHA-EA (p = 0.013) whereas no changes were seen with the other diets. Lowering dietary LA did not result in the expected changes in fatty acids associated with the LA-ARA inflammatory axis in women with overweight and obesity.

Lipids are one of the cell components therefore it is important to be able to accurately assess them. One of the analytical techniques used to study lipid profiles is matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI TOF MS). The present study attempted to select optimal conditions for sample preparation and MALDI MS analysis of bacterial lipidome in both positive and negative ion modes using different extraction protocols—Folch, Matyash, and Bligh & Dyer, solvents used to apply samples, and matrices such as 9-aminoacridine (9-AA), α-cyano-4-hydroxycinnamic acid (CHCA), 2,5-dihydroxybenzoic acid (DHB), 2-mercaptobenzothiazole (MBT), and 2,4,6-trihydroxyacetophenone (THAP). The obtained results allowed concluding that DHB or CHCA matrices are suitable for lipid analysis in the positive mode, and in the negative mode THAP or 9-AA. The most appropriate protocol for extracting lipids from bacterial cells was the Bligh & Dyer method in both ionization modes. The use of the solvent TA30, which was a mixture of acetonitrile and 0.1% trifluoroacetic acid in water, provided on the spectra a significant number of signals from lipids in all groups analyzed, such as fatty acyls, glycerolipids, and glycerophospholipids.

Consumption of a Western diet (WD) is known to increase the risk of obesity. Short or medium chain fatty acids influence energy metabolism, and triacetin, a synthetic short chain triacylglyceride, has been shown to lower body fat under normal conditions. This study aimed to investigate if triacetin as part of a WD modifies rat weight and body fat. Male rats were fed a control diet or WD for 8 weeks. At week 8, rats in the WD group were maintained on a WD diet or switched to a WD diet containing 30% energy from medium-chain triacylglyceride (WD-MCT) or triacetin (WD-T) for another 8 weeks. At week 16, rats were euthanized and liver, adipose and blood were collected. Tissue fatty acids (FAs) were quantified by gas chromatography (GC) and hepatic FAs were measured by GC-combustion-isotope ratio mass spectrometry for δ¹³C-palmitic acid (PAM)—a novel marker of de novo lipogenesis (DNL). Rats fed WD-T had a body weight not statistically different to the control group, and gained less body weight than rats fed WD alone. Furthermore, WD-T fed rats had a lower fat mass, and lower total liver and plasma FAs compared to the WD group. Rats fed WD-T did not differ from WD in blood ketone or glucose levels, however, had a significantly lower hepatic δ¹³C-PAM value than WD fed rats; suggestive of lower DNL. In summary, we show that triacetin has the potential to blunt weight gain and adipose tissue accumulation in a rodent model of obesity, possibly due to a decrease in DNL.

Liver inflammation has become increasingly prevalent in recent years, leading to the development of diseases like hepatitis, alcoholic liver disease, and fatty liver disease. One factor that has been linked to liver inflammation is increased levels of lipopolysaccharides (LPS), which can be caused by poor diets and sedentary lifestyles that contribute to liver inflammation. There is promising research on a new class of lipids called fatty acid esters of hydroxy fatty acids (FAHFAs), which have been shown to potentiate insulin release and exert an anti-inflammatory effect. Specifically, one type of FAHFA called 9-POHSA (palmitoleic acid ester of 9-hydroxy stearic acid) has been studied for its potential to attenuate inflammation-related indexes induced by LPS in hepatocytes, which play a critical role in the progression of liver inflammation. This study found that following LPS treatment, tumor necrosis factor- α, interleukin-6, and connective tissue growth factor (CTGF) were upregulated and increased cell migration, but 9-POHSA pre-treatment attenuated the upregulation of these markers and prevented cell migration induced by LPS. Using flowcytometry analysis, intracellular reactive oxygen species (ROS) was found to be responsible for CTGF upregulation. In addition, the effects of 9-POHSA were likely associated with its inhibition of the activation of the NF-kB. These results suggest that 9-POHSA has potential as a therapy for liver inflammation and fibrosis by attenuating inflammation-related indexes induced by LPS in hepatocytes. This study provides important insight into the mechanisms of liver inflammation and the potential for new treatments to address liver diseases.

Shakeri, H, Hadaegh, H, Abedi, F, Tajabadi-Ebrahimi, M, Mazroii, N, Ghandi, Y and Asemi, Z. Consumption of synbiotic bread decreases triacylglycerol and VLDL levels while increasing HDL levels in serum from patients with type-2 diabetes. Lipids. 2014;49:695–701. https://doi.org/10.1007/s11745-014-3901-z.

The journal is aware of a number of issues raised regarding the integrity of research published by Zatolleh Asemi and colleagues (Grey et al., 2020). An investigation into these concerns has been conducted by The National Committee for Ethics in Biomedical Research Iran, in coordination with Kashan University of Medical Sciences (KAUMS). The Editor has independently considered the concerns reported for this article and did not find evidence of questionable research practices at this time. The following corrections have therefore been made.

In the above-referenced published article, the study was reported to have taken place between October 2013 and December 2013. This is an apparent error in the preparation of the manuscript. The correct timing of the study was between December 2013 and January 2014. In the published article Figure 1 and Tables 1, 2, and 3 state that the number of participants for which samples were analyzed was 26. This is a systematic typographical error; the correct number is 24 participants. The authors neglected to acknowledge the contribution to the study of Drs. Maryam Tajabadi-Ebrahimi and Haleh Hadaegh. The correct version of the acknowledgment should therefore be: Acknowledgments: The present study was supported by a Grant (No. 92107) from the Vice-Chancellor for Research, KAUMS, Kashan, Iran. The authors would like to thank the staff of Gholabchi Clinic (Kashan, Iran) for their assistance in this project. We are grateful to the Research and Development Department of Sahar Bread Company, Tehran, Iran that provided probiotic and synbiotic products for the present study. Furthermore, we are grateful to the Research and Development Department of Tak Gene Zist Company, Tehran, Iran that provided Lactobacillus sporogenes for this study. The authors wish to acknowledge the contributions of Drs. Maryam Tajabadi-Ebrahimi and Haleh Hadaegh who conducted the analysis of the blood samples. The authors apologize for any inconvenience these errors and oversights may have caused.