Lipids in Health and Disease
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Published By Springer (Biomed Central Ltd.)

1476-511x, 1476-511x
Updated Tuesday, 14 September 2021

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Kenjiro Tatematsu ◽  
Daisuke Miyazawa ◽  
Yoshiaki Saito ◽  
Harumi Okuyama ◽  
Naoki Ohara

Abstract Background Canola oil (Can) and several vegetable oils shorten the lifespan of stroke-prone spontaneously hypertensive rats (SHRSP). Although similar lifespan shortening has been reported for partially hydrogenated Can, the efficacy of fully hydrogenated oils on the lifespan remains unknown. The present study aimed to investigate the lifespan of SHRSP fed diets containing 10 % (w/w) of fully hydrogenated Can (FHCO) or other oils. Methods Survival test: Upon weaning, male SHRSP were fed a basal diet for rodents mixed with one of the test oils —i.e., FHCO, Can, lard (Lrd), and palm oil (Plm) throughout the experiment. The animals could freely access the diet and drinking water (water containing 1 % NaCl), and their body weight, food intake, and lifespan were recorded. Biochemical analysis test: Male SHRSP were fed a test diet with either FHCO, Can, or soybean oil (Soy) under the same condition, except to emphasize effects of fat, that no NaCl loading was applied. Soy was used as a fat source in the basal diet and was set the control group. Blood pressures was checked every 2 weeks, and serum fat levels and histological analyses of the brain and kidney were examined after 7 or 12 weeks of feeding. Results During the survival study period, the food consumption of FHCO-fed rats significantly increased (15–20 % w/w) compared with that of rats fed any other oil. However, the body weight gain in the FHCO group was significantly less (10–12 %) than that in the control group at 9–11 weeks old. The FHCO (> 180 days) intervention had the greatest effect on lifespan, followed by the Lrd (115 ± 6 days), Plm (101 ± 2 days), and Can (94 ± 3 days) diets. FHCO remarkably decreased the serum cholesterol level compared with Can and the systolic blood pressure from 12 to 16 weeks of age. In addition, while some rats in the Can group exhibited brain hemorrhaging and renal dysfunction at 16 weeks old, no symptoms were observed in the FHCO group. Conclusion This current study suggests that complete hydrogenation decreases the toxicity of Can and even prolongs the lifespan in SHRSP.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Ryuichi Kawamoto ◽  
Asuka Kikuchi ◽  
Taichi Akase ◽  
Daisuke Ninomiya ◽  
Teru Kumagi

Abstract Background Low-density lipoprotein cholesterol (LDL-C) independently impacts aging-related health outcomes and plays a critical role in cardiovascular diseases (CVDs). However, there are limited predictive data on all-cause mortality, especially for the Japanese community population. In this study, it was examined whether LDL-C is related to survival prognosis based on 7 or 10 years of follow-up. Methods Participants included 1610 men (63 ± 14 years old) and 2074 women (65 ± 12 years old) who participated in the Nomura cohort study conducted in 2002 (first cohort) and 2014 (second cohort) and who continued throughout the follow-up periods (follow-up rates: 94.8 and 98.0%). Adjusted relative risk estimates were obtained for all-cause mortality using a basic resident register. The data were analyzed by a Cox regression with the time variable defined as the length between the age at the time of recruitment and that at the end of the study (the age of death or censoring), and risk factors including gender, age, body mass index (BMI), presence of diabetes, lipid levels, renal function, serum uric acid levels, blood pressure, and history of smoking, drinking, and CVD. Results Of the 3684 participants, 326 (8.8%) were confirmed to be deceased. Of these, 180 were men (11.2% of all men) and 146 were women (7.0% of all women). Lower LDL-C levels, gender (male), older age, BMI under 18.5 kg/m2, and the presence of diabetes were significant predictors for all-cause mortality. Compared with individuals with LDL-C levels of 144 mg/dL or higher, the multivariable-adjusted Hazard ratio (and 95% confidence interval) for all-cause mortality was 2.54 (1.58–4.07) for those with LDL-C levels below 70 mg/dL, 1.71 (1.15–2.54) for those with LDL-C levels between 70 mg/dL and 92 mg/dL, and 1.21 (0.87–1.68) for those with LDL-C levels between 93 mg/dL and 143 mg/dL. This association was particularly significant among participants who were male (P for interaction = 0.039) and had CKD (P for interaction = 0.015). Conclusions There is an inverse relationship between LDL-C levels and the risk of all-cause mortality, and this association is statistically significant.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Ryuk Jun Kwon ◽  
Eun-Ju Park ◽  
Sang Yeoup Lee ◽  
Youngin Lee ◽  
Chungsu Hwang ◽  
...  

Abstract Background Colorectal cancer (CRC) is a malignancy of the large intestine, whose development and prognosis have been demonstrated to be associated with altered lipid metabolism. High cholesterol intake is associated with an increased risk of CRC, and elevated serum cholesterol levels are known to be correlated with risk of developing CRC. Niemann-Pick C1-Like 1 (NPC1L1), a target of ezetimibe, plays an essential role in the absorption of intestinal cholesterol. However, whether the altered expression of NPC1L1 affects CRC development and prognosis is currently unknown. Methods Data corresponding to patients with CRC were obtained from The Cancer Genome Atlas (TCAG). Datasets from the Genome Data Analysis Center (GDAC) platform were analyzed to compare the expression of NPC1L1 in normal and CRC tissues using the Mann–Whitney U test and chi-square test. Further, the datasets from the Gene Expression Omnibus (GEO) database were analyzed. The log-rank test and multivariate Cox proportional hazard regression analysis were performed to determine whether NPC1L1 significantly affects the prognosis of CRC. Results The expression of NPC1L1 was found to be upregulated in CRC and was significantly associated with the N and pathological stages but not with the histological type, age, and sex. Increased NPC1L1 expression in CRC was related to poor patient survival, as evidenced by the Kaplan–Meier and multivariate regression analyses. Conclusions As high expression of NPC1L1 was associated with CRC development, pathological stage, and prognosis, NPC1L1 can serve as an independent prognostic marker for CRC.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Haochang Hu ◽  
Ruoyu Chen ◽  
Yingchu Hu ◽  
Jian Wang ◽  
Shaoyi Lin ◽  
...  

Abstract Background As an autosomal dominant disorder, familial hypercholesterolemia (FH) is mainly attributed to disease-causing variants in the low-density lipoprotein receptor (LDLR) gene. The aim of this study was to explore the molecular mechanism of LDLR c.501C>A variant in FH and assess the efficacy of proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitor treatment for FH patients. Methods The whole-exome sequencing was performed on two families to identify disease-causing variants, which were verified by Sanger sequencing. The function of LDLR variant was further explored in HEK293 cells by Western Blot and confocal microscopy. Besides, the therapeutic effects of PCSK9 inhibitor treatment for two probands were assessed for 3 months. Results All members of the two families with the LDLR c.501C>A variant showed high levels of LDLC. The relationship between the clinical phenotype and LDLR variants was confirmed in the current study. Both in silico and in vitro analyses showed that LDLR c.501C>A variant decreased LDLR expression and LDL uptake. PCSK9 inhibitor treatment lowered the lipid level in proband 1 by 24.91%. However, the treatment was ineffective for proband 2. A follow-up study revealed that the PCSK9 inhibitor treatment had low ability of lipid-lowering effect in the patients. Conclusions LDLR c.501C>A variant might be pathogenic for FH. The PCSK9 inhibitor therapy is not a highly effective option for treatment of FH patients with LDLR c.501C>A variant.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Haoqiang Zhang ◽  
Wenwen Zhu ◽  
Tong Niu ◽  
Zheng Wang ◽  
Ke An ◽  
...  

Abstract Background Low-density lipoprotein cholesterol (LDL-C) metabolic disorder is common in individuals with diabetes. The role of LDL-C in mild cognitive impairment (MCI) remains to be explored. We aim to investigate the associations between LDL-C at different levels and details of cognition decline in patients with type 2 diabetes mellitus (T2DM). Methods Patients with T2DM (n = 497) were recruited. Clinical parameters and neuropsychological tests were compared between patients with MCI and controls. Goodness of fit was assessed to determine the linear or U-shaped relationship between LDL-C and cognitive function. The cut-off point of LDL-C was calculated. Correlation and regression were carried out to explore the relationship between cognitive dysfunction and LDL-C levels above and below the cut-off point. Results Although no significant difference in LDL-C levels was detected in 235 patients with MCI, compared with 262 patients without MCI, inverted-U-shaped association was determined between LDL-C and Montreal Cognitive Assessment (MoCA). The cut-off point of LDL-C is 2.686 mmol/l. LDL-C (>2.686 mmol/l) is positively related to Trail Making Test B (TMTB) indicating executive function. LDL-C (<2.686 mmol/l) is positively associated with Clock Drawing Test (CDT) reflecting visual space function in patients with T2DM. Conclusion Inverted U-shaped correlation was found between serum LDL-C and cognitive function in patients with T2DM. Despite that the mechanisms of different LDL-C levels involved in special cognitive dysfunctions remain incompletely clarified, excessive LDL-C damages executive function, while the deficient LDL-C impairs visual space function. Trial registration ChiCTR-OCC-15006060.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Fei Gao ◽  
Zhi Jian Wang ◽  
Xiao Teng Ma ◽  
Hua Shen ◽  
Li Xia Yang ◽  
...  

Abstract Background Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors have been demonstrated to produce significantly greater reduction in LDL cholesterol levels and cardiovascular events than standard statin therapy. However, evidence on the impact of PCSK9 inhibitors on coronary plaque composition and morphology is limited. Methods In this open-label randomized study, eligible patients with intermediate coronary lesions and elevated LDL cholesterol values were randomized to either alirocumab 75 mg Q2W plus statin (atorvastatin 20 mg/day or rosuvastatin 10 mg/day) therapy or standard care. Optical coherence tomography (OCT) assessments for target lesions were obtained at baseline and at 36 weeks of follow-up. Results LDL cholesterol levels were significantly decreased in both the alirocumab and standard care arms, whereas the absolute reduction in LDL cholesterol was significantly greater in patients treated with alirocumab (1.72 ± 0.51 vs. 0.96 ± 0.59, P < 0.0001). Compared with standard care, the addition of alirocumab to statins was associated with significantly greater increases in minimum fibrous cap thickness (18.0 [10.8–29.2] μm vs 13.2 [7.4–18.6] μm; P = 0.029), greater increases in minimum lumen area (0.20[0.10–0.33] mm2 vs 0.13 [0.12–0.24] mm2; P = 0.006) and a greater diminution in maximum lipid arc (15.1̊ [7.8–24.5] vs. 8.4̊ [2.0–10.5]; P = 0.008). Conclusions The addition of alirocumab to statins can not only provide additional LDL cholesterol lowering effects but also have a potential role in promoting a more stable plaque phenotype. Trial registration ClinicalTrials.gov Identifier: NCT04851769. Registered 2 Mar 2019.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Szu-Wei Huang ◽  
Yu-Che Ou ◽  
Kuo-Shu Tang ◽  
Hong-Ren Yu ◽  
Li-Tung Huang ◽  
...  

Abstract Background The deleterious effect of maternal high-fat diet (HFD) on the fetal rat liver may cause later development of non-alcoholic fatty liver disease (NAFLD). The aim of this study was to evaluate the effect of maternal HFD-induced maternal hepatic steatosis and dysbiosis on the fetal liver and intestines, and the effect of prenatal metformin in a rat model. Methods Sprague–Dawley rats were assigned to three groups (N = 6 in each group). Before mating, the rats were randomly assigned to HFD or normal-chow diet (NCD) group for 7 weeks. After mating, the HFD group rats were continued with high-fat diet during pregnancy and some of the HFD group rats were co-treated with metformin (HFMf) via drinking water during pregnancy. All maternal rats and their fetuses were sacrificed on gestational day 21. The liver and intestinal tissues of both maternal and fetal rats were analyzed. In addition, microbial deoxyribonucleic acid extracted from the maternal fecal samples was analyzed. Results HFD resulted in maternal weight gain during pregnancy, intrahepatic lipid accumulation, and change in the serum short-chain fatty acid profile, intestinal tight junctions, and dysbiosis in maternal rats. The effect of HFD on maternal rats was alleviated by prenatal metformin, which also ameliorated inflammation and apoptosis in the fetal liver and intestines. Conclusions This study demonstrated the beneficial effects of prenatal metformin on maternal liver steatosis, focusing on the gut-liver axis. In addition, the present study indicates that prenatal metformin could ameliorate maternal HFD-induced inflammation and apoptosis in the fetal liver and intestines. This beneficial effect of in-utero exposure of metformin on fetal liver and intestines has not been reported. This study supports the use of prenatal metformin for pregnant obese women.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Xiaoyu Wang ◽  
Jingdong Liu ◽  
Zongyou Cheng ◽  
Yanjia Zhong ◽  
Xiaohua Chen ◽  
...  

Abstract Background Triglyceride glucose-body mass index (TyG-BMI) has been proven to be a reliable substitute for insulin resistance. However, whether a causal association exists between TyG-BMI and new-onset diabetes remains uncertain. The purpose of this study was to investigate the causal association and predictive performance between TyG-BMI and diabetes. Methods A total of 116,661 subjects who underwent a physical examination were included in this study. The subjects were divided into five equal points according to the quintile of TyG-BMI, and the outcome of interest was the occurrence of diabetic events. TyG-BMI = ln [fasting plasma glucose (mg/dL) × fasting triglycerides (mg/dL)/2] × BMI. Results During the average follow-up period of 3.1 (0.95) years, 1888 men (1.61 %) and 793 women (0.68 %) were newly diagnosed with diabetes. Multivariate Cox regression analysis showed that TyG-BMI was an independent predictor of new-onset diabetes (HR 1.50 per SD increase, 95 %CI: 1.40 to 1.60, P-trend < 0.00001), and the best TyG-BMI cutoff value for predicting new-onset diabetes was 213.2966 (area under the curve 0.7741, sensitivity 72.51 %, specificity 69.54 %). Additionally, the results of subgroup analysis suggested that the risk of TyG-BMI-related diabetes in young and middle-aged people was significantly higher than that in middle-aged and elderly people, and the risk of TyG-BMI-related diabetes in non-obese people was significantly higher than that in overweight and obese people (P for interaction < 0.05). Conclusions This cohort study of the Chinese population shows that after excluding other confounding factors, there is a causal association of TyG-BMI with diabetes, and this independent association is more obvious in young, middle-aged and non-obese people.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Amanda J. Berberich ◽  
Alexandra M. Ouédraogo ◽  
Salimah Z. Shariff ◽  
Robert A. Hegele ◽  
Kristin K. Clemens

Abstract Background The incidence of severe (S-HTG) and very severe hypertriglyceridemia (VS-HTG) among Canadians is unknown. This study aimed to determine the incidence, characteristics, predictors and care patterns for individuals with VS-HTG. Methods Using linked administrative healthcare databases, a population-based cohort study of Ontario adults was conducted to determine incidence of new onset S-HTG (serum triglycerides (TG) > 10–20 mmol/L) and VS-HTG (TG > 20 mmol/L) between 2010 and 2015. Socio-demographic and clinical characteristics of those with VS-HTG were compared to those who had no measured TG value > 3 mmol/L. Univariable and multivariable logistic regression were used to determine predictors for VS-HTG. Healthcare patterns were evaluated for 2 years following first incidence of TG > 20 mmol/L. Results Incidence of S-HTG and VS-HTG in Ontario was 0.16 and 0.027% among 10,766,770 adults ≥18 years and 0.25 and 0.041% among 7,040,865 adults with at least one measured TG, respectively. Predictors of VS-HTG included younger age [odds ratios (OR) 0.64/decade, 95% confidence intervals (CI) 0.62–0.66], male sex (OR 3.83; 95% CI 3.5–4.1), diabetes (OR 5.38; 95% CI 4.93–5.88), hypertension (OR 1.69; 95% CI 1.54–1.86), chronic liver disease (OR 1.71; 95% CI 1.48–1.97), alcohol abuse (OR 2.47; 95% CI 1.90–3.19), obesity (OR 1.49; 95% CI 1.13–1.98), and chronic kidney disease (OR 1.39; 95% CI 1.19–1.63). Conclusion The 5-year incidence of S-HTG and VS-HTG in Canadian adults was 1 in 400 and 1 in 2500, respectively. Males, those with diabetes, obese individuals and those with alcohol abuse are at highest risk for VS-HTG and may benefit from increased surveillance.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yukai Xiang ◽  
Xiangyu Kong ◽  
Cheng Zhang ◽  
Chuanqi He ◽  
Jingli Cai ◽  
...  

Abstract Background Pancreaticobiliary reflux (PBR) causes chronic inflammation of the gallbladder mucosa and changes in the bile components, which are known to promote gallstone formation. This study aimed to investigate the bile biochemistry changes in gallstone patients with PBR and provide new clues for research on the involvement of PBR in gallstone formation. Methods Patients undergoing surgery for gallstones between December 2020 and May 2021 were eligible for inclusion. The bile biochemistry (including amylase, lipase, triglyceride, cholesterol, free fatty acids [FFAs], alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase [ALP], and γ-glutamyl transferase [γ-GT]) of the included gallstone patients was analysed to determine correlations with PBR. Results In this study, 144 gallstone patients who underwent surgery were enrolled. Overall, 15.97 % of the patients had an increased bile amylase level, which was associated with older age and significantly higher bile levels of ALP, lipase, triglyceride, and FFAs. Positive correlations were observed between amylase and lipase, triglyceride, FFAs levels in the gallbladder bile. However, the bile levels of triglyceride, FFAs, and lipase were positively correlated with each other only in the PBR group and showed no significant correlation in the control (N) group. In addition, elevated bile FFAs levels were found to be an independent risk factor for gallbladder wall thickening. Conclusions In conclusion, PBR-induced increase in FFAs and triglyceride in the gallbladder bile is a cause of gallstone formation, and an increase in bile ALP suggests the presence of cholestasis in PBR.


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