Melatonin alleviates cognition impairment by antagonizing brain insulin resistance in aged rats fed a high-fat diet.

Brain insulin resistance, induced by neuroinflammation and oxidative stress, contributes to neurodegeneration, that is, processes that are associated with Aß accumulation and TAU hyperphosphorylation. Here, we tested the effect of chronic administration of melatonin (MLT) on brain insulin resistance and cognition deficits caused by a high-fat diet (HFD) in aged rats. Results showed that MLT supplementation attenuated peripheral insulin resistance and lowered hippocampal oxidative stress levels. Activated microglia and astrocytes and hippocampal levels of TNF-α in HFD-fed rats were reduced by MLT treatment. Melatonin also prevented HFD-induced increases in beta-amyloid (Aß) accumulation and TAU phosphorylation in the hippocampus. In addition, impairments of brain insulin signaling elicited by long-term HFD were restored by MLT treatment, as confirmed by ex vivo insulin stimulation. Importantly, MLT reversed HFD-induced cognitive decline as measured by a water maze test, normalized hippocampal LTP and restored CREB activity and BDNF levels as well as cholinergic neuronal activity in the hippocampus. Collectively, these findings indicate that MLT may exhibit substantial protective effects on cognition, via restoration of brain insulin signaling.

Lipingshu capsule improves atherosclerosis associated with lipid regulation and inflammation inhibition in apolipoprotein E-deficient mice.

BACKGROUND: Atherosclerosis (AS) is mainly responsible for cardiovascular diseases. The present study investigated whether Lipingshu capsule (LPS), whose ingredients are present in health food stores, has beneficial effect on AS. METHODS: C57BL/6 J mice were given a low fat rodent diet and assigned as control group (CON). ApoE-/- mice were placed on high fat rodent diet and randomly separated into high fat diet (HFD) group and HFD + LPS group whose animals were given 0.9 g/kg.BW LPS daily for 10 weeks. Atherosclerotic lesions in aorta and aortic root were evaluated. Serum lipids and multiple cytokine were measured. RESULTS: ApoE-/- mice fed with high fat diet had serious aortic lesions, whereas LPS markedly decreased plaque area of the total aorta and of the aortic root. LPS recovered the serum lipid profiles by substantially reducing TC, LDL-C, TG and Ox-LDL contents. Multi-cytokine analysis revealed greater serum levels of IL-1α, IL-1ß, IL-6, IFN-γ, GMCSF, RANTES and TNF-α induced by high fat diet slumped with LPS treatment. CONCLUSION: LPS reduces atherosclerotic lesions and thus alleviates AS by lipid profile modulation and inflammation inhibition.

Chronic alpha-linolenic acid treatment alleviates age-associated neuropathology: Roles of PERK/eIF2α signaling pathway.

Aging is a principal risk factor for neurodegenerative diseases and especially shares similar pathologic mechanisms to Alzheimer's disease (AD). Amyloid-ß (Aß) plaques deposition and neurofibrillary tangles (NFTs) are the prominent age-dependent pathologies implicated in the cognitive deficits. Accumulation of mis-folded proteins in the endoplasmic reticulum triggers a cellular stress response called the unfolded protein response (UPR), the activation of which is increased in AD patients. However, the UPR relates to the pathological hallmarks of aging is still elusive. In this study, we report that long-term supplement of α-linolenic acid (ALA), starting before the onset of disease symptoms (6month-old), prevents the age-related memory deficits during natural aging. The amelioration of the memory impairment is associated with a decrease in UPR related markers [glucose regulated protein 78 (GRP78), protein kinase RNA-like endoplasmic reticulum kinase (PERK), eukaryotic Initiation Factor 2α (eIF2α)]. ALA suppressed the PERK/eIF2α signaling, which may be responsible for multifaceted memory-deteriorating and neurodegenerative mechanisms, including inhibition of Aß production by suppressing ß-site APP-cleaving enzyme 1 (BACE1) expression, enhancement of cAMP response element binding protein (CREB) function via down-regulating activating transcription factor 4 (ATF4), and suppression of Tau phosphorylation by inhibiting glycogen synthase kinase 3ß (GSK-3ß) pathway. Taken together, our findings provide new insights into the link between ALA and PERK/eIF2α signaling, which could contribute to a better understanding of an ALA-mediated protective effect in aging-associated neuropathology.

Single frequency intake of α-linolenic acid rich phytosterol esters attenuates atherosclerosis risk factors in hamsters fed a high fat diet.

BACKGROUND: Emerging evidence suggested phytosterol esters (PE) exhibited an advantage over naturally occurring phytosterols in reducing atherosclerosis risk factors due to improved fat solubility and compatibility. However, the effects of dietary patterns of PE on lipid-lowering activity were limited and inconsistent. This study aimed to explore the effects of dose and frequency of α-linolenic acid rich phytosterol esters (ALA-PE) on cholesterol and triglyceride metabolism markers focused on intestinal cholesterol absorption and bioconversion of ALA in liver. METHODS: Dose-dependency study Male Syrian golden hamsters were fed high-fat diets (HFD) containing low, medium and high dose of ALA-PE (0.72 %, 2.13 % and 6.39 %) for 6 weeks. The high fat diet contained 89.5 % chow diet, 0.2 % cholesterol, 10 % lard and 0.3 % bile salt. Dose-frequency study Male Syrian golden hamsters were provided: (I) 0.4 mL/100 g peanut oil by gavage once a day; (II) 0.4 mL/100 g ALA-PE by gavage once a day; (III) 0.2 mL/100 g ALA-PE by gavage twice a day; (IV) 0.133 mL/100 g ALA-PE by gavage three times a day; (V) 0.1 mL/100 g ALA-PE by gavage four times a day for 6 weeks with a high-fat diet simultaneously. RESULTS: ALA-PE dose-dependently lowered plasma total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) concentrations with a maximal decrease of 42 %, 59 % and 73 %, respectively (p < 0.05). Compared to HFD, TC, LDL-C and TG concentrations were significantly lower (p < 0.01) in hamsters consumed HFD plus ALA-PE for 1-4 times per day but there were not remarkable differences among different consumption frequencies. No significant changes in plasma antioxidant capacity and lipid peroxidation levels were observed among HFD and HFD plus different doses of ALA-PE groups. The contents of hepatic α-linolenic (ALA), docosapentaenoic (DPA) and docosahexaenoic (DHA) acids were dose-dependently increased in different ALA-PE groups compared to those in HFD group. The abundance of mRNA for intestinal sterol transporters Niemann-Pick C1-Like 1 (NPC1L1), ATP-binding cassette (ABC) transporters ABCG5 and ABCG8 indicated no significant differences among all groups. CONCLUSION: ALA-PE dose-dependently improved lipid profile in hamsters fed HFD independent of intestinal ABCG5, ABCG8 and NPC1L1, accompanying by increased conversion of ALA to DPA and DHA in liver. ALA-PE manifested "once a day" lipid-lowering efficacy, highlighting a promising preventive strategy for metabolic syndrome.

Effects of endogenous and exogenous micronutrients in rapeseed oils on the antioxidant status and lipid profile in high-fat fed rats.

BACKGROUND: Micronutrients in oil reduce one or more risk factors of cardiovascular diseases, while the contents of micronutrients in oil are relatively poor, which is insufficient to reverse the metabolic disorders at different stages of progress. The aim of this study was to investigate the effects of endogenous micronutrients in optimized cold-pressed rapeseed oil and restoratively added or fortified micronutrients in traditional refined rapeseed oil (restoring micronutrients to be nearly equal to or significantly higher than levels in crude rapeseed oil) on the antioxidant status and lipid profile in high-fat fed rats. METHODS: Male Wistar rats were fed high-fat diets containing different rapeseed oils for 4 weeks, including the standard refined rapeseed oil(SRO), optimized cold-pressed rapeseed oil(CRO) and the traditional refined rapeseed oil with restorative addition or fortification of micronutrients (LF, HF-SRO). RESULTS: CRO exhibited significant increases in contents of tocopherols (+13%), phytosterols (+34%), polyphenols (+92%) and phospholipids (+725%) compared with SRO, as well as the total antioxidant capacities (+82-125%) (p<0.05). While the HF-SRO revealed improved antioxidant properties in vitro than the CRO, which was comparable to LF-SRO. Significant improved plasma antioxidant capacities and lipid peroxidation evaluated by T-AOC, GSH, tocopherols and MDA were found in rats fed HF-SRO when compared with CRO and LF-SRO (p<0.05). Furthermore, HF-SRO also decreased the plasma and hepatic TC levels compared to CRO and LF-SRO, accompanying higher fecal cholesterol excretion (p<0.05). CONCLUSION: The standard refined rapeseed oil with fortification, not restorative addition of micronutrients was comparable to the optimized cold-pressed rapeseed oil in improving the antioxidant status and lipid profile of high-fat fed rats.

A combination of flaxseed oil and astaxanthin alleviates atherosclerosis risk factors in high fat diet fed rats.

BACKGROUND: Atherosclerosis is the most common pathologic process underlying cardiovascular disease. Both flaxseed oil (FO) and astaxanthin (ASX) are believed to benefit cardiovascular system. The combined effect of FO and ASX on the atherosclerosis risk factors in rats fed a high-fat diet was investigated. METHODS: Astaxanthin was dissolved in flaxseed oil to a final concentration of 1g/kg (FO + ASX). Male Sprague-Dawley rats were fed a rodent diet contained 20% fat whose source was lard (HFD) or 75% lard and 25% FO + ASX (50 mg ASX/kg diet) or 50% lard and 50% FO + ASX (100 mg ASX/kg diet) or FO + ASX (200 mg ASX/kg diet) for 10 weeks. RESULTS: The combination of FO and ASX significantly increased the antioxidant defense capacity and decreased lipid peroxidation in plasma. Evident decreases in the levels TG, TC and LDL-C contents, as well as IL-6 and CRP were also observed in plasma of FO and ASX fed rats. CONCLUSION: The combination of FO and ASX can improve oxidative stress, lipid abnormalities and inflammation, providing evidence that the combination of FO and ASX could be a promising functional food in cardiovascular health promotion.

Optimized rapeseed oils rich in endogenous micronutrients ameliorate risk factors of atherosclerosis in high fat diet fed rats.

BACKGROUND: Micronutrients in rapeseed such as polyphenols, tocopherols, phytosterols and phospholipids in rapeseed exert potential benefit to atherosclerosis. Some part of these healthy components substantially lost during the conventional refining processing. Thus some new processing technologies have been developed to produce various endogenous micronutrient-enriched optimized rapeseed oils. The aim of this study is to assess whether optimized rapeseed oils have positive effects on the atherosclerosis risk factors in rats fed a high-fat diet. METHODS: Rats received experiment diets containing 20% fat and refined rapeseed oil or optimized rapeseed oils obtained with various processing technologies as lipid source. After 10 weeks of treatment, plasma was assayed for oxidative stress, lipid profiles and imflammation. RESULTS: Micronutrients enhancement in optimized rapeseed oils significantly reduced plasma oxidative stress, as evaluated by the significant elevation in the activities of CAT and GPx as well as the level of GSH, and the significant decline in lipid peroxidation. Optimized rapeseed oil with the highest micronutrient contents obtained by microwave pretreatment-cold pressing reduced the levels of TG, TC and LDL-C as well as IL-6 and CRP in plasma. CONCLUSIONS: These results suggest that optimized rapeseed oils may contribute to prevent atherogenesis and make them very promising functional food in cardiovascular health promotion.

Defective ferritinophagy and imbalanced iron metabolism in PBDE-47-triggered neuronal ferroptosis and salvage by Canolol.

The brominated flame retardant 2,2',4,4'-tetrabromodiphenyl ether (PBDE-47) is a ubiquitous environmental pollutant that causes neurotoxicity. However, incomplete understanding of the underlying mechanisms has hampered the development of effective intervention strategies. Oxidative stress and related cell death are the modes of action for PBDE-47 neurotoxicity, which are also the characteristics of ferroptosis. Nonetheless, the role of ferroptosis in PBDE-47-induced neurotoxicity remains unclear. In the present study, we found that PBDE-47 triggered ferroptosis in neuron-like PC12 cells, as evidenced by intracellular iron overload, lipid peroxidation, and mitochondrial damage. This was confirmed by ferroptosis inhibitors including the lipid reactive oxygen species scavenger ferrostatin-1 and iron chelator deferoxamine mesylate. Mechanistically, PBDE-47 impaired ferritinophagy by disrupting nuclear receptor coactivator 4-mediated lysosomal degradation of the iron storage protein ferritin. Moreover, PBDE-47 disturbed iron metabolism by increasing cellular iron import via upregulation of transferrin receptor 1 and decreasing cellular iron export via downregulation of ferroportin 1 (FPN1). Intriguingly, rescuing lysosomal function by overexpressing cathepsin B (CatB) mitigated PBDE-47-induced ferroptosis by partially restoring dysfunctional ferritinophagy and enhancing iron excretion via the upregulation of FPN1. However, FPN1 knockdown reversed the beneficial effects of CatB overexpression on the PBDE-47-induced iron overload. Finally, network pharmacology integrated with experimental validation revealed that Canolol, the main phenolic compound in canola oil, protected against PBDE-47-evoked iron overload, resulting in ferroptosis by restoring defective ferritinophagy and improving abnormal iron metabolism via lowering iron uptake and facilitating iron excretion. Overall, these data suggest that ferroptosis is a novel mechanism of PBDE-47-induced neuronal death and that manipulation of ferritinophagy and iron metabolism via Canolol represents a promising therapeutic strategy.

Micronutrients-fortified rapeseed oil improves hepatic lipid accumulation and oxidative stress in rats fed a high-fat diet.

Intake of high-fat diet is associated with increased fatty livers. Hepatic lipid accumulation and oxidative stress are key pathophysiological mechanisms in this disease. Micronutrients polyphenols, tocopherols and phytosterols in rapeseed exert potential benefit to hepatoprotection, but most of these micronutrients are removed by the traditional refining process. The purpose of the present study was to determine whether rapeseed oil fortified with these micronutrients can decrease hepatic lipid accumulation and oxidative stress induced by high-fat diet. Sprague-Dawley rats received rodent diet contained 20% fat whose source was refined rapeseed oil (RRO) or fortified RRO with low, middle and high quantities of these micronutrients for 10 weeks. Intake of RRO caused a remarkable hepatic steatosis. Micronutrients supplementation was effective in reducing steatosis as well as total triglyceride and total cholesterol contents in liver. These micronutrients also significantly increased hepatic antioxidant defense capacities, as evaluated by the significant elevation in the activities of SOD and GPx as well as the level of GSH, and the significant decline in lipid peroxidation. These findings suggest that rapeseed oil fortified with micronutrients polyphenols, tocopherols and phytosterols may contribute to prevent fatty livers such as nonalcoholic fatty liver disease by ameliorating hepatic lipid accumulation and oxidative stress.

Flaxseed oil and alpha-lipoic acid combination ameliorates hepatic oxidative stress and lipid accumulation in comparison to lard.

BACKGROUND: Intake of high-fat diet is associated with increased non-alcoholic fatty liver disease (NAFLD). Hepatic lipid accumulation and oxidative stress are key pathophysiological mechanisms in NAFLD. Both flaxseed oil (FO) and α-lipoic acid (LA) exert potential benefit to NAFLD. The aim of this study was to determine the effect of the combination of FO and LA on hepatic lipid accumulation and oxidative stress in rats induced by high-fat diet. METHODS: LA was dissolved in flaxseed oil to a final concentration of 8 g/kg (FO + LA). The rodent diet contained 20% fat. One-fifth of the fat was soybean oil and the others were lard (control group), or 75% lard and 25% FO + LA (L-FO + LA group), or 50% lard and 50% FO + LA (M-FO + LA group), or FO + LA (H-FO + LA group). Male Sprague-Dawley rats were fed for 10 weeks and then killed for liver collection. RESULTS: Intake of high-fat lard caused a significant hepatic steatosis. Replacement with FO + LA was effective in reducing steatosis as well as total triglyceride and total cholesterol contents in liver. The combination of FO and LA also significantly elevated hepatic antioxidant defense capacities, as evaluated by the remarkable increase in the activities of SOD, CAT and GPx as well as the level of GSH, and the significant decline in lipid peroxidation. CONCLUSION: The combination of FO and LA may contribute to prevent fatty livers such as NAFLD by ameliorating hepatic lipid accumulation and oxidative stress.

Docosahexaenoic acid enhances hippocampal insulin sensitivity to promote cognitive function of aged rats on a high-fat diet.

INTRODUCTION: Diminished brain insulin sensitivity is associated with reduced cognitive function. Docosahexaenoic acid (DHA) is known to maintain normal brain function. OBJECTIVES: This study aimed to determine whether DHA impacts hippocampal insulin sensitivity and cognitive function in aged rats fed a high-fat diet (HFD). METHODS: Eight-month-old female Sprague-Dawley rats were randomly divided into three groups (n = 50 each). Rats in the aged group, HFD group, and DHA treatment group received standard diet (10 kcal% fat), HFD (45 kcal% fat), and DHA-enriched HFD (45 kcal% fat, 1% DHA, W/W) for 10 months, respectively. Four-month-old female rats (n = 40) that received a standard diet served as young controls. Neuroinflammation, oxidative stress, amyloid formation, and tau phosphorylation in the hippocampus, as well as systemic glucose homeostasis and cognitive function, were tested. RESULTS: DHA treatment relieved a block in the insulin signaling pathway and consequently protected aged rats against HFD-induced hippocampal insulin resistance. The beneficial effects were explained by a DHA-induced decrease in systemic glucose homeostasis dysregulation, hippocampal neuroinflammation and oxidative stress. In addition, DHA treatment broke the reciprocal cycle of hippocampal insulin resistance, Aß burden, and tau hyperphosphorylation. Importantly, treatment of model rats with DHA significantly increased their cognitive capacity, as evidenced by their increased hippocampal-dependent learning and memory, restored neuron morphology, enhanced cholinergic activity, and activated cyclic AMP-response element-binding protein. CONCLUSION: DHA improves cognitive function by enhancing hippocampal insulin sensitivity.

Saccharomyces boulardii protects against murine experimental colitis by reshaping the gut microbiome and its metabolic profile.

Introduction: Saccharomyces boulardii (S. boulardii) has shown clinical beneficial effect in inflammatory bowel diseases recently. However, the underlying mechanisms remain incompletely understood. The aim of present study was to tested whether S. boulardii targets gut microbiota to protect against the development of experimental colitis in mice. Methods: Female C57BL/6 mice were gavaged with S. boulardii for 3 weeks before being challenged with dextran sulphate sodium to induce ulcerative colitis. Bodyweight, diarrhea severity, intestinal permeability, colonic histopathology, colonic inflammatory status, and epithelial cell death of mice were examined. The fecal microbiota and its metabolomic profiles were detected by 16S rDNA sequencing and UPLC-MS, respectively. Results and Discussion: Supplementation with S. boulardii significantly prevented weight loss and colon shortening, lowered colonic inflammation, ameliorated epithelial injury, and enhanced the intestinal barrier integrity in colitis mice. By inhibiting the abundance of pathogenic bacteria and increasing the probiotics abundance, S. boulardii improved the microbial diversity and restored the microbiota dysbiosis. Moreover, it also modulated microbial metabolome and altered the relative contents of metabolites involving amino acids, lipids, energy and vitamin metabolisms. These yeast-driven shifts in gut flora and metabolites are were associated with each other and with the inflammation profile in colitis. Collectively, S. boulardii exerts protective effects on colitis in mice by reshaping gut microbiome and its metabolic profile, indicating it as a promising therapeutic avenue.

Flaxseed oil and α-lipoic acid combination reduces atherosclerosis risk factors in rats fed a high-fat diet.

BACKGROUND: Atherosclerosis is a major manifestation of the pathophysiology underlying cardiovascular disease. Flaxseed oil (FO) and α-lipoic acid (LA) have been reported to exert potential benefit to cardiovascular system. This study tried to assess the effect of supplement of FO and LA combination on the atherosclerosis risk factors in rats fed a high-fat diet. METHODS: LA was dissolved in flaxseed oil to a final concentration of 8 g/kg (FO+LA) when used. The rodent diet contained 20% fat. One-fifth of the fat was soybean oil and the others were lard (HFD group), or 75% lard and 25% FO+LA (L-FO+LA group), or 50% lard and 50% FO+LA (M-FO+LA group), or FO+LA (H-FO+LA group). Animals were fed for 10 weeks and then killed for blood collection. RESULTS: Supplement of FO and LA combination significantly enhanced plasma antioxidant defense capacities, as evaluated by the marked increase in the activities of SOD, CAT and GPx as well as the level of GSH, and the significant reduction in lipid peroxidation. Simultaneous intake of FO and LA also reduced plasma TG, TC and LDL-C contents and elevated the ratio of HDL-C/LDL-C. Besides, in parallel with the increase of FO and LA combination, plasma IL-6 and CRP levels were remarkably reduced. CONCLUSION: Supplement of FO and LA combination may contribute to prevent atherogenesis by improving plasma oxidative stress, lipid profile and inflammation.

Effects of flaxseed oil on anti-oxidative system and membrane deformation of human peripheral blood erythrocytes in high glucose level.

BACKGROUND: The erythrocyte membrane lesion is a serious diabetic complication. A number of studies suggested that n-3 fatty acid could reduce lipid peroxidation and elevate α- or γ-tocopherol contents in membrane of erythrocytes. However, evidence regarding the protective effects of flaxseed oil, a natural product rich in n-3 fatty acid, on lipid peroxidation, antioxidative capacity and membrane deformation of erythrocytes exposed to high glucose is limited. METHODS: Human peripheral blood erythrocytes were isolated and treated with 50 mM glucose to mimic hyperglycemia in the absence or presence of three different doses of flaxseed oil (50, 100 or 200 µM) in the culture medium for 24 h. The malondialdehyde (MDA) and L-glutathione (GSH) were measured by HPLC and LC/MS respectively. The phospholipids symmetry and membrane fatty acid composition of human erythrocytes were detected by flow cytometry and gas chromatograph (GC). The morphology of human erythrocyte was illuminated by ultra scanning electron microscopy. RESULTS: Flaxseed oil attenuated hyperglycemia-induced increase of MDA and decrease of GSH in human erythrocytes. Human erythrocytes treated with flaxseed oil contained higher C22:5 and C22:6 than those in the 50 mM glucose control group, indicating that flaxseed oil could reduce lipid asymmetric distribution and membrane perturbation. The ultra scanning electron microscopy and flow cytometer have also indicated that flaxseed oil could protect the membrane of human erythrocytes from deformation at high glucose level. CONCLUSION: The flaxseed oil supplementation may prevent lipid peroxidation and membrane dysfunction of human erythrocytes in hyperglycemia.

Laxative effects of partially defatted flaxseed meal on normal and experimental constipated mice.

BACKGROUND: Constipation is a very common health problem in the world. Intake of sufficient amount of dietary fibers is a cornerstone in the prevention and treatment of constipation. As a traditional medicine, flaxseed has been used to treat constipation for centuries, but the controlled trials are rare. The purpose of the present study was to assess that whether partially defatted flaxseed meal (PDFM) has the potential role to facilitate fecal output in normal and experimental constipated mice. METHODS: After supplemented with 2.5%, 5% and 10% (w/w) PDFM (L-, M- and H-PDFM) for 14 days, the constipation models of mice were induced by atropine-diphenoxylate. The small intestinal transit rates, start time of defecation, amount of defecation and wet weight of feces were researched in normal and constipation model mice. RESULTS: M- and H-PDFM significantly increase small intestinal transit rates in constipation model mice. All dose of PDFM markedly shortened the start time of defecation and M- and H-PDFM significantly increase stool frequency and weight in both normal and constipation model mice. CONCLUSIONS: PDFM may be a useful laxative to facilitate fecal output in normal and constipation conditions.

Rapeseed oil fortified with micronutrients reduces atherosclerosis risk factors in rats fed a high-fat diet.

BACKGROUND: Micronutrients polyphenols, tocopherols and phytosterols in rapeseed exert potential benefit to cardiovascular system, but most of these micronutrients are removed by the refining process. The aim of this study was to determine the effect of rapeseed oil fortified with these micronutrients on the atherosclerosis risk factors in rats fed a high-fat diet. METHODS: The rodent diet contained 20% fat whose source was refined rapeseed oil (RRO) or fortified refined rapeseed oil with low, middle and high quantities of these micronutrients (L-, M- and H-FRRO). Forty male SD rats were divided into four groups. One group received RRO diet and other groups received L-, M- and H-FRRO diet for 10 weeks. RESULTS: Micronutrients supplementation significantly increased plasma antioxidant defense capacities, as evaluated by the significant elevation in the activities of GPx, CAT and SOD as well as the level of GSH, and the significant decline in lipid peroxidation. These micronutrients also reduced the plasma contents of TG, TC and LDL-C and increased the ratio of HDL-C/LDL-C. In addition, in parallel with the enhancement of these micronutrients, plasma levels of IL-6 and CRP declined remarkably. CONCLUSION: Rapeseed oil fortified with micronutrients polyphenols, tocopherols and phytosterols may contribute to prevent atherogenesis by ameliorating plasma oxidative stress, lipid profile and inflammation.

Serumal Lipidomics Reveals the Anti-inflammatory Effect of Flax Lignans and Sinapic Acid in High-Fat-Diet-Fed Mice.

Flax lignans (SDG) and sinapic acid (SA) both have the function of antioxidation and anti-inflammation. However, previous studies have focused mainly on biochemical measurements, gene expression analysis, and clinical assessments. There are limited studies that systematically reveal the underlying mechanism of the anti-inflammation effect of SDG or SA from the lipidomic point of view. Herein, the integrated lipidomic profiling platform was used for the analysis of free fatty acids (FFAs), phospholipids (PLs), triacylglycerols (TAGs), and oxylipins in high-fat (HF)-diet-fed mice after SDG or SA administration. Dietary supplementation of SDG or SA downregulated the levels of total TAGs and FFAs in the ApoE-/- mice model. Furthermore, 28 potential lipids were screened out and considered as key evaluation factors to understand the anti-inflammation function and mechanism of SDG and SA. The results indicated that the anti-inflammatory effect of SDG and SA was principally exerted via regulation of lipid homeostasis.

Highlights of the Fifth International Symposium on Lipid Science and Health.

The International Symposium on Lipid Science and Health (ISLSH) has been organized annually by the Oil Crops Research Institute of Chinese Academy of Agricultural Sciences (OCRI-CAAS) since 2016. The purpose of the symposium was to bring together the leading lipid science and health researchers throughout the world to discuss the current state of knowledge as well as research needs with respect to chemistry and beneficial health properties of lipids. The Fifth International Symposium on Lipid Science and Health was held on October 2020 in Wuhan, Hubei, China. Speakers from China, the United States, Australia, Finland, and other countries delivered wonderful presentations. The presentations covered such diverse topics as lipid profiling and characterization, lipid preparation and modification, lipid improvement and regulation, and lipid nutrition and health. As a record of the symposium proceedings, this special issue comprises a selection of 27 papers from oral presentations and poster contributions and is prefaced by this introduction.

Association between heme oxygenase-1 gene promoter polymorphisms and type 2 diabetes mellitus: a HuGE review and meta-analysis.

Several studies have recently focused on the association between heme oxygenase-1 (HMOX1) gene promoter polymorphisms and susceptibility to type 2 diabetes mellitus; however, results have been conflicting. This systematic Human Genome Epidemiology review and meta-analysis was undertaken to integrate previous findings and summarize the effect size of the association of HMOX1 gene promoter polymorphisms with susceptibility to type 2 diabetes. The authors retrieved all studies matched to search terms from the PubMed/MEDLINE, EMBASE, and ISI Web of Science databases that had been published through December 31, 2009. The articles were then checked independently by 2 investigators according to the eligibility and exclusion criteria. For all alleles and genotypes, odds ratios were pooled using either fixed-effects or random-effects models. An increased odds ratio for type 2 diabetes was observed in persons with the (GT)(n) L (long) allele as compared with those with the (GT)(n) S (short) allele (odds ratio = 1.12, 95% confidence interval: 1.02, 1.24; P = 0.02). Furthermore, the diabetes odds ratio for persons with the LL genotype, versus those with the SS genotype, was significantly increased (odds ratio = 1.25, 95% confidence interval: 1.04, 1.50; P = 0.02). Persons carrying longer (GT)(n) repeats in the HMOX1 gene promoter may have a higher risk of type 2 diabetes.

Procyanidins extracted from the lotus seedpod ameliorate scopolamine-induced memory impairment in mice.

The major purpose of this study was to determine the effect of procyanidins extracted from the lotus seedpod (LSPC) on the learning and memory impairments induced by scopolamine (1 mg/kg, i.p.) in mice. The capacities of memory and learning were evaluated by the Morris water maze and the step-down avoidance test. LSPC (50, 100, 150 mg/kg BW, p.o.) significantly reversed scopolamine-induced learning and memory impairments in the Morris water maze test, as evaluated by shortened escape latency and swimming distance. In the step-down avoidance test, LSPC (50, 100, 150 mg/kg BW, p.o.) treatment significantly reduced the number of errors and shortened latency compared with that of scopolamine. In addition, LSPC was also found to inhibit acetyl cholinesterase (AChE) activity. These results of this study suggest that LSPC may play a useful role in the treatment of cognitive impairment caused by AD and aging.