linoleic-acid and Metabolic-Syndrome

Linoleic acid (LA) is a major constituent of low-density lipoproteins. An essential fatty acid, LA is a polyunsaturated fatty acid, which is oxidised by endogenous enzymes and reactive oxygen species in the circulation. Increased levels of low-density lipoproteins coupled with oxidative stress and lack of antioxidants drive the oxidative processes. This results in synthesis of a range of oxidised derivatives, which play a vital role in regulation of inflammatory processes. The derivatives of LA include, hydroxyoctadecadienoic acids, oxo-​octadecadienoic acids, epoxy octadecadecenoic acid and epoxy-keto-octadecenoic acids. In this review, we examine the role of LA derivatives and their actions on regulation of inflammation relevant to metabolic processes associated with atherogenesis and cancer. The processes affected by LA derivatives include, alteration of airway smooth muscles and vascular wall, affecting sensitivity to pain, and regulating endogenous steroid hormones associated with metabolic syndrome. LA derivatives alter cell adhesion molecules, this initial step, is pivotal in regulating inflammatory processes involving transcription factor peroxisome proliferator-activated receptor pathways, thus, leading to alteration of metabolic processes. The derivatives are known to elicit pleiotropic effects that are either beneficial or detrimental in nature hence making it difficult to determine the exact role of these derivatives in the progress of an assumed target disorder. The key may lie in understanding the role of these derivatives at various stages of development of a disorder. Novel pharmacological approaches in altering the synthesis or introduction of synthesised LA derivatives could possibly help drive processes that could regulate inflammation in a beneficial manner. Chemical Compounds: Linoleic acid (PubChem CID: 5280450), 9- hydroxyoctadecadienoic acid (PubChem CID: 5312830), 13- hydroxyoctadecadienoic acid (PubChem CID: 6443013), 9-oxo-​octadecadienoic acid (PubChem CID: 3083831), 13-oxo-​octadecadienoic acid (PubChem CID: 4163990), 9,10-epoxy-12-octadecenoate (PubChem CID: 5283018), 12,13-epoxy-9-keto-10- trans -octadecenoic acid (PubChem CID: 53394018), Pioglitazone (PubChem CID: 4829).

Topics: Animals; Fatty Acids, Unsaturated; Humans; Inflammation; Linoleic Acid; Metabolic Syndrome; Neoplasms; Oxidation-Reduction

Essential fatty acids (EFAs)--linoleic acid (LA) and alpha-linolenic acid (ALA) are critical for human survival. EFAs are readily available in the diet. But, to derive their full benefit, EFAs need to be metabolized to their respective long-chain metabolites. EFAs not only form precursors to respective prostaglandins (PGs), thromboxanes (TXs), and leukotrienes (LTs), but also give rise to lipoxins (LXs), resolvins, isoprostanes, and hydroxy- and hydroperoxyeicosatetraenoates. Certain PGs, TXs, and LTs have pro-inflammatory actions whereas LXs and resolvins are anti-inflammatory in nature. Furthermore, EFAs and their long-chain metabolites modulate the activities of angiotensin converting and HMG-CoA reductase enzymes, enhance acetylcholine levels in the brain, increase the synthesis of endothelial nitric oxide, augment diuresis, and enhance insulin action. Thus, EFAs and their metabolites may function as endogenous ACE and HMG-CoA reductase inhibitors, nitric oxide enhancers, beta-blockers, diuretics, anti-hypertensive, and anti-atherosclerotic molecules. In addition, EFAs and their long-chain metabolites react with nitric oxide (NO) to yield respective nitroalkene derivatives that exert cell-signaling actions via ligation and activation of peroxisome proliferator-activated receptors (PPARs). Thus, EFAs and their derivatives have varied biological actions that may have relevance to their involvement in several physiological and pathological processes.

Topics: alpha-Linolenic Acid; Arteriosclerosis; Fatty Acids, Essential; Humans; Inflammation; Linoleic Acid; Metabolic Syndrome

Data from a number of studies and trials have shown that different conjugated linoleic acids (CLA's) may produce beneficial effects on cancer, atherosclerosis, hypertension, diabetes and changes in body composition. Despite the increasing knowledge about CLA's implications on health, the mechanism of action of these fatty acids is not completely understood. Moreover, human studies indicate that some of these beneficial effects are considerably less evident than anticipated from mice studies, while the efficacy and safety of dietary supplements containing CLA have been questioned in some intervention trials. Recently, it has been suggested that the anti-carcinogenic and anti-atherosclerosis effects of CLA's stem from its anti-inflammatory properties. Because inflammatory responses are associated with the pathophysiology of many diseases, including obesity and the metabolic syndrome, the investigation in this area is of growing interest in recent years.

Topics: Anti-Inflammatory Agents; Humans; Inflammation; Linoleic Acid; Metabolic Syndrome; Obesity; Oxidative Stress

The health benefits of substituting dietary polyunsaturated fatty acids (PUFAs) for saturated fatty acids are well known. However, limited information exists on how the response to dietary intake of linoleic acid (LA; 18:2n-6) is modified by polymorphisms in the fatty acid desaturase (FADS) gene cluster.. The aim of the current study was to test the hypothesis that the FADS1 rs174550 genotype modifies the effect of dietary LA intake on the fatty acid composition of plasma lipids, fasting glucose, and high-sensitivity C-reactive protein (hsCRP).. Associations were investigated between genotype, plasma PUFAs, fasting glucose, and hsCRP concentrations in the cross-sectional, population-based Metabolic Syndrome in Men cohort (n = 1337). In addition, 62 healthy men from the cohort who were homozygotes for the TT or CC genotype of the FADS1 rs174550 were recruited to a 4-wk intervention (FADSDIET) with an LA-enriched diet. The fatty acid composition of plasma PUFAs and concentrations of plasma fasting glucose, serum hsCRP, and plasma lipid mediators (eicosanoids and related analogs) were measured at the beginning and end of the 4-wk intervention period.. In the FADSDIET trial, the plasma LA proportion increased in both genotype groups in response to an LA-enriched diet. Responses in concentrations of serum hsCRP and plasma fasting glucose and the proportion of arachidonic acid (20:4n-6) in plasma phospholipids and cholesteryl esters differed between genotype groups (interaction of diet × genotype, P < 0.05). In TT homozygous subjects, plasma eicosanoid concentrations correlated with the arachidonic acid proportion in plasma and with hsCRP (r = 0.4-0.7, P < 0.05), whereas in the CC genotype there were no correlations.. Our findings show that the FADS1 genotype modifies metabolic responses to dietary LA. The emerging concept that personalized dietary counseling should be modified by the FADS1 genotype needs to be tested in larger randomized trials. The study was registered at clinicaltrials.gov as NCT02543216.

Topics: Aged; Blood Glucose; C-Reactive Protein; Cross-Sectional Studies; Delta-5 Fatty Acid Desaturase; Diet; Fasting; Fatty Acid Desaturases; Fatty Acids; Fatty Acids, Omega-6; Fatty Acids, Unsaturated; Finland; Genotype; Homozygote; Humans; Inflammation; Linoleic Acid; Lipids; Male; Metabolic Syndrome; Middle Aged; Polymorphism, Single Nucleotide

Plant-derived α-linolenic acid (ALA) may exert cardioprotective effects. Dietary ALA can undergo desaturation and elongation to form long-chain ω-3 polyunsaturated fatty acids, but the extent to which this occurs in humans is unclear. The aim of the study was to examine the effects of an energy-restricted diet enriched with ALA on fatty acid composition of serum phospholipids in patients with metabolic syndrome.. The present analysis compared the effects of a hypoenergetic diet high in ALA (3.4 g/d) with a control diet low in ALA (0.9 g/d) on fatty acid composition of serum phospholipids in 81 overweight or obese patients with features of metabolic syndrome.. After a 26-wk intervention, concentration of ALA in serum phospholipids remained constant in both diet groups. The control group had a significant decrease in serum phospholipid eicosapentaenoic acid concentration, although no significant intergroup difference was observed. Serum phospholipid docosahexaenoic acid concentration significantly decreased to a similar extent with both interventions. Additionally, both interventions significantly decreased serum phospholipid concentrations of palmitic acid, stearic acid, total saturated fatty acids, linoleic acid, total ω-6 and ω-3 polyunsaturated fatty acids, with no effect of diet group on these changes. Compared with the ALA diet, the control diet led to a significant increase in serum phospholipid oleic acid concentration.. Daily intake of 3.4 g of ALA during a 26-wk energy-restricted diet did not lead to an enrichment of serum phospholipids with ALA and did not increase eicosapentaenoic acid due to conversion. Additionally, dietary ALA was unable to compensate for a decrease in serum phospholipid docosahexaenoic acid.

Topics: Adult; Aged; alpha-Linolenic Acid; Caloric Restriction; Diet; Dietary Fats; Fatty Acids; Female; Humans; Linoleic Acid; Male; Metabolic Syndrome; Middle Aged; Obesity; Overweight; Phospholipids; Young Adult

Conjugated linoleic acid (CLA) is a group of dietary fatty acids with antiobesity and antidiabetic effects in some animals. The trans10cis12 (t10c12) CLA isomer seems to cause these effects, including improved insulin sensitivity. Whether such isomer-specific effects occur in humans is unknown. The aim of this study was to investigate whether t10c12 CLA or a commercial CLA mixture could improve insulin sensitivity, lipid metabolism, or body composition in obese men with signs of the metabolic syndrome.. In a randomized, double-blind controlled trial, abdominally obese men (n = 60) were treated with 3.4 g/day CLA (isomer mixture), purified t10c12 CLA, or placebo. Euglycemic-hyperinsulinemic clamp, serum hormones, lipids, and anthropometry were assessed before and after 12 weeks of treatment.. Baseline metabolic status was similar between groups. Unexpectedly, t10c12 CLA increased insulin resistance (19%; P < 0.01) and glycemia (4%; P < 0.001) and reduced HDL cholesterol (-4%; P < 0.01) compared with placebo, whereas body fat, sagittal abdominal diameter, and weight decreased versus baseline, but the difference was not significantly different from placebo. The CLA mixture did not change glucose metabolism, body composition, or weight compared with placebo but lowered HDL cholesterol (-2%; P < 0.05).. These results reveal important isomer-specific metabolic actions of CLA in abdominally obese humans. A CLA-induced insulin resistance has previously been described only in lipodystrophic mice. Considering the use of CLA-supplements among obese individuals, it is important to clarify the clinical consequences of these results, but they also provide physiological insights into the role of specific dietary fatty acids as modulators of insulin resistance in humans.

Topics: Adult; Aged; Body Composition; Diabetes Mellitus; Double-Blind Method; Humans; Hyperlipidemias; Insulin Resistance; Isomerism; Leptin; Linoleic Acid; Lipoproteins; Male; Metabolic Syndrome; Middle Aged; Obesity

We aimed to explore the mechanism of the linoleic acid metabolism in metabolic syndrome (MetS). RNA-seq data for 16 samples with or without MetS from the GSE145412 dataset were collected. Gene set variation analysis (GSVA), gene set enrichment analysis (GSEA), and gene differential expression analysis were performed. Expression data of differentially expressed genes (DEGs) involved in the linoleic acid metabolism pathway were mapped to the pathway by using Pathview for visualization. There were 19 and 10 differentially expressed biological processes in the disease group and healthy group, respectively. 9 KEGG pathways were differentially expressed in the disease group. Linoleic acid metabolism was the only differentially expressed pathway in the healthy group. The GSVA enrichment score of the linoleic acid metabolism pathway in the disease group was markedly lower than that in the healthy group. The GSEA result showed that the linoleic acid metabolism pathway was significantly downregulated in the disease group. JMJD7-PLA2G4B, PLA2G1B, PLA2G2D, CYP2C8, and CYP2J2 involved in the pathway were significantly downregulated in the disease group. This study may provide novel insight into MetS from the point of linoleic acid metabolism dysregulation.

Topics: Biochemical Phenomena; Gene Expression Profiling; Humans; Linoleic Acid; Metabolic Syndrome; Transcriptome

Not all obese individuals develop cardiovascular disease (CVD). Hyperaldosteronism is suggested to cause inflammation and metabolic dysregulation, and might contribute to CVD development in obese individuals.. We aimed to investigate the association of aldosterone concentrations with inflammation, metabolic disturbances, and atherosclerosis in overweight and obese individuals. Additionally, we measured renin concentrations to investigate whether the observed effects reflected general activation of the renin-angiotensin-aldosterone system (RAAS).. A cross-sectional cohort study (300-OB study) was conducted. Various inflammatory parameters, traits of the metabolic syndrome, lipidome and metabolome parameters, fat distribution, and carotid atherosclerosis were associated with plasma aldosterone and renin levels.. The setting of this study was the Radboudumc (i.o. Radboudumc), the Netherlands.. A total of 302 individuals with a body mass index greater than or equal to 27 kg/m2 participated.. Aldosterone was associated with various markers of inflammation and metabolic dysregulation, which partly differed from the associations observed for renin. Although both were associated with inflammatory cell numbers, only renin was associated with classical markers of systemic inflammation. Both were associated with the metabolic syndrome and hepatic steatosis. Of the traits that constitute metabolic syndrome, aldosterone, but not renin, was associated with triglyceride concentrations. Accordingly, aldosterone was associated with large very low-density lipoprotein particles; metabolomics studies further associated aldosterone with urate concentrations and derivatives of the linoleic acid metabolism pathway. Neither aldosterone nor renin was associated with atherosclerotic plaque thickness.. Aldosterone is not an important driver of systemic inflammation in the obese, whereas aldosterone concentrations and metabolic dysregulation are strongly intertwined in these individuals. Although prospective studies are necessary to validate these results, the independent effects of aldosterone on carotid atherosclerosis appear modest.

Topics: Aged; Aged, 80 and over; Aldosterone; Atherosclerosis; Biomarkers; Carotid Arteries; Cross-Sectional Studies; Fasting; Female; Humans; Hyperaldosteronism; Inflammation; Linoleic Acid; Lipoproteins, VLDL; Magnetic Resonance Imaging; Male; Metabolic Syndrome; Metabolomics; Middle Aged; Netherlands; Obesity; Renin; Triglycerides

Fatty acid desaturase 1 (

Topics: Adult; alpha-Linolenic Acid; Cross-Sectional Studies; Delta-5 Fatty Acid Desaturase; Diet, Vegetarian; Fatty Acid Desaturases; Female; Humans; Linoleic Acid; Malaysia; Male; Metabolic Syndrome; Middle Aged; Polymorphism, Single Nucleotide; Risk Assessment; Risk Factors; Vegetarians

We tested whether oxidized linoleic acid metabolites (OXLAM) are associated with pediatric metabolic syndrome (MetS) and a proatherogenic lipoprotein profile in 122 obese adolescents. Furthermore, we examined whether genetic and metagenomic factors can modulate plasma OXLAM concentrations by genotyping the

Topics: Adolescent; Age Factors; Biomarkers; Child; Delta-5 Fatty Acid Desaturase; Disease Susceptibility; Fatty Acid Desaturases; Female; Gastrointestinal Microbiome; Genetic Background; Genetic Predisposition to Disease; Haplotypes; Humans; Linoleic Acid; Lipid Metabolism; Lipoproteins; Male; Metabolic Syndrome; Metabolome; Obesity; Oxidation-Reduction

Uncoupling proteins (UCPs) are members of the mitochondrial anion carrier superfamily involved in the control of body temperature and energy balance regulation. They are currently proposed as therapeutic targets for treating obesity and metabolic syndrome (MetS). We studied the gene expression regulation of UCP1, -2, and -3 in abdominal white adipose tissue (WAT) from control and MetS rats treated with two doses of a commercial mixture of resveratrol (RSV) and quercetin (QRC). We found that UCP2 was the predominantly expressed isoform, UCP3 was present at very low levels, and UCP1 was undetectable. The treatment with RSV + QRC did not modify UCP3 levels; however, it significantly increased UCP2 mRNA in control and MetS rats in association with an increase in oleic and linoleic fatty acids. WAT from MetS rats showed a significantly increased expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ when compared to the control group. Furthermore, PPAR-α protein levels were increased by the highest dose of RSV + QRC in the control and MetS groups. PPAR-γ expression was only increased in the control group. We conclude that the RSV + QRC treatment leads to overexpression of UCP2, which is associated with an increase in MUFA and PUFA, which might increase PPAR-α expression.

Topics: Adipose Tissue, White; Animals; Gene Expression Regulation; Insulin; Linoleic Acid; Male; Metabolic Syndrome; Mitochondrial Uncoupling Proteins; Oleic Acid; Peroxisome Proliferator-Activated Receptors; Quercetin; Radioimmunoassay; Rats; Rats, Wistar; Resveratrol; RNA, Messenger; Stilbenes; Uncoupling Protein 1; Uncoupling Protein 2; Uncoupling Protein 3

The causes of the multiple metabolic disorders of individuals with chronic kidney disease (CKD) are not fully known. We investigated the relationships between dietary fat quality, the metabolic syndrome (MetS), insulin sensitivity and inflammation in individuals with CKD.. Two population-based surveys were conducted in elderly Swedish individuals (aged 70 years) with serum cystatin C-estimated glomerular filtration rate <60 mL min(-1) /1.73 m2: the Uppsala Longitudinal Study of Adult Men (ULSAM) and the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) surveys. The present population comprised 274 men and 187 subjects (63% women) from the ULSAM and PIVUS cohorts, respectively.. Factor analyses of serum fatty acids were used to evaluate dietary fat quality. Insulin sensitivity was measured by homeostasis model assessment of insulin resistance (IR) and, in ULSAM, also by euglycaemic clamp.. Factor analyses generated two fatty acid patterns of (i) low linoleic acid (LA)/high saturated fatty acid (SFA) or (ii) high n-3 polyunsaturated fatty acid (n-3 PUFA) levels. In both surveys, the low LA/high SFA pattern increased the odds of having MetS [adjusted odds ratio 0.60 [95% confidence interval (CI) 0.44-0.81] and 0.45 (95% CI 0.30-0.67) per SD decrease in factor score in the ULSAM and PIVUS surveys, respectively] and was directly associated with both IR and C-reactive protein. The n-3 PUFA pattern was not consistently associated with these risk factors.. A serum fatty acid pattern reflecting low LA and high SFA was strongly associated with MetS, IR and inflammation in two independent surveys of elderly individuals with CKD. At present, there are no specific dietary guidelines for individuals with CKD; however, these findings indirectly support current recommendations to replace SFAs with PUFAs from vegetable oils.

Topics: Aged; Aged, 80 and over; Dietary Fats; Fatty Acids; Female; Glomerular Filtration Rate; Glucose Clamp Technique; Health Surveys; Humans; Inflammation; Insulin Resistance; Linoleic Acid; Longitudinal Studies; Male; Metabolic Syndrome; Middle Aged; Renal Insufficiency, Chronic; Sweden

Because alterations in blood fatty acid (FA) composition by dietary lipids are associated with insulin resistance and related metabolic disorders, we hypothesized that serum phospholipid FA composition would reflect the early alteration of fasting glycemic status, even in people without metabolic syndrome (MetS). To examine this hypothesis, serum phospholipid FA, desaturase activities, fasting glycemic status, and cardiometabolic parameters were measured in study participants (n = 1022; 30-69 years; male, n = 527; female, n = 495; nondiabetics without disease) who were stratified into normal fasting glucose (NFG) and impaired fasting glucose (IFG) groups. Total monounsaturated FA (MUFA), oleic acid (OA; 18:1n-9), dihomo-γ-linolenic acid (DGLA; 20:3n-6), Δ-9-desaturase activity (D9D; 18:1n-9/18:0), and DGLA/linoleic acid (20:3n-6/18:2n-6) in serum phospholipids were significantly higher in IFG subjects than NFG controls. Study subjects were subdivided into 4 groups, based on fasting glucose levels and MetS status. Palmitoleic acid (16:1n-7) was highest in IFG-MetS and lowest in NFG-non-MetS subjects. Oleic acid and D9D were higher in IFG-MetS than in the other 3 groups. Dihomo-γ-linolenic acid and DGLA/linoleic acid were higher in MetS than in non-MetS, regardless of fasting glucose levels. The high-sensitivity C-reactive proteins (hs-CRPs) and 8-epi-prostaglandin-F2α were higher in IFG than in NFG, regardless of MetS status. Oxidized low-density lipoproteins were higher in IFG-MetS than in the other 3 groups. Total MUFAs, OA, and D9D were positively correlated with homeostasis model assessment of insulin resistance, fasting glucose, triglyceride, hs-CRP, and 8-epi-prostaglandin-F2α. Palmitoleic acid was positively correlated with triglyceride and hs-CRP. Lastly, total MUFA, OA, palmitoleic acid, and D9D were associated with early alteration of fasting glycemic status, therefore suggesting that these may be useful markers for predicting the risk of type 2 diabetes and cardiometabolic diseases.

Topics: 8,11,14-Eicosatrienoic Acid; Biomarkers; Blood Glucose; C-Reactive Protein; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Dinoprost; Fasting; Fatty Acids, Monounsaturated; Female; Humans; Insulin; Insulin Resistance; Linoleic Acid; Lipoproteins, LDL; Male; Metabolic Syndrome; Middle Aged; Oleic Acid; Phospholipids; Stearoyl-CoA Desaturase; Triglycerides

Environmental contaminants have previously been linked to components of the Metabolic Syndrome (MetS). However, exposure to environmental contaminants is in part determined by various lifestyle factors.. Using an "Environmental Wide Association Study" (ELWAS) integrating environmental contaminants and lifestyle factors, we aimed to evaluate a possible additive role of both contaminants and lifestyle factors regarding MetS.. 1016 subjects aged 70years were investigated in the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study. 43 environmental contaminants were measured in the circulation. Dietary records were used to evaluate 21 nutrients and the proportions of 13 fatty acids were determined in serum cholesterol esters to further quantify fat quality intake. Adding 5 other important lifestyle factors yielded together 76 environmental and lifestyle factors. MetS was defined by the NCEP/ATPIII-criteria.. 23% had MetS. Using cross-validation within the sample, fourteen environmental contaminants or lifestyle factors consistently showed a false discovery rate <0.05. When the major variables entered a multiple model, only p, p'-DDE levels (positive), PCB209 (inverse) and exercise habits (inverse) were together with a fatty acid pattern, with high levels of palmitic acid and oleic acid and low levels of linoleic acid, related to MetS (p<0.002 for all variables).. Using a cross-sectional EWAS approach, certain environmental contaminants and lifestyle factors were found to be associated with prevalent metabolic syndrome in an additive fashion in an elderly population.

Topics: Aged; Cholesterol; Cross-Sectional Studies; Environmental Exposure; Environmental Pollutants; Fatty Acids; Female; Humans; Life Style; Linoleic Acid; Male; Metabolic Syndrome; Prevalence; Prospective Studies

We investigated the changes in adiposity, cardiovascular and liver structure and function, and tissue fatty acid compositions in response to oleic acid-rich macadamia oil, linoleic acid-rich safflower oil and α-linolenic acid-rich flaxseed oil (C18 unsaturated fatty acids) in rats fed either a diet high in simple sugars and mainly saturated fats or a diet high in polysaccharides (cornstarch) and low in fat. The fatty acids induced lipid redistribution away from the abdomen, more pronounced with increasing unsaturation; only oleic acid increased whole-body adiposity. Oleic acid decreased plasma total cholesterol without changing triglycerides and nonesterified fatty acids, whereas linoleic and α-linolenic acids decreased plasma triglycerides and nonesterified fatty acids but not cholesterol. α-Linolenic acid improved left ventricular structure and function, diastolic stiffness and systolic blood pressure. Neither oleic nor linoleic acid changed the left ventricular remodeling induced by high-carbohydrate, high-fat diet, but both induced dilation of the left ventricle and functional deterioration in low fat-diet-fed rats. α-Linolenic acid improved glucose tolerance, while oleic and linoleic acids increased basal plasma glucose concentrations. Oleic and α-linolenic acids, but not linoleic acid, normalized systolic blood pressure. Only oleic acid reduced plasma markers of liver damage. The C18 unsaturated fatty acids reduced trans fatty acids in the heart, liver and skeletal muscle with lowered stearoyl-CoA desaturase-1 activity index; linoleic and α-linolenic acids increased accumulation of their C22 elongated products. These results demonstrate different physiological and biochemical responses to primary C18 unsaturated fatty acids in a rat model of human metabolic syndrome.

Topics: Absorptiometry, Photon; Adipose Tissue; Animals; Body Composition; Dietary Carbohydrates; Dietary Fats; Glucose Tolerance Test; Linoleic Acid; Linolenic Acids; Liver; Male; Metabolic Syndrome; Muscle, Skeletal; Oleic Acid; Rats; Rats, Wistar

The fatty acid composition of high-fat diets is known to influence the magnitude of postprandial events that increase the risk of metabolic syndrome. These variations in magnitude may be directly ascribed to differences in the channeling of lipids toward oxidation or storage. A study was designed to compare the effects of 4 dietary fats on postprandial energy expenditure and on some risk factors of the metabolic syndrome. To avoid usual confounding factors due to simultaneous variations in chain length and double-bounds number of fatty acids, dietary fats were chosen to provide mainly 18-carbon fatty acids with 0 (stearic acid [SA]), 1 (oleic acid [OA]), 2 (linoleic acid [LA]), or 3 (alpha-linolenic acid [ALA]) double bounds. They were given as single high-fat test meals to 4 different groups of male rats. The resting metabolic rate and the lipid and carbohydrate oxidation were measured from oxygen consumption and carbon dioxide production using indirect calorimetry 2 hours before and 6.5 hours after the test meal. Plasma glucose, triglyceride, and chylomicron concentrations were determined at 0, 1.5, and 4 hours after the test meal. Postprandial concentration of glucose and triglyceride did not vary with the nature of the test meals, whereas that of chylomicrons was the highest after the LA test meal and the lowest after the SA test meal. Postprandial increase in resting metabolic rate was the highest after the LA and OA test meals, and the lowest after the SA and ALA test meals. Compared with the 3 other diets, the ALA test meal enhanced lipid oxidation and decreased glucose oxidation during the early postprandial period (0.25-3.25 hours). This suggests that stearic acid may not induce all the adverse effects classically described for other saturated fatty acids and that alpha-linolenic acid may beneficially influence energy partitioning, especially during the early postprandial state.

Topics: alpha-Linolenic Acid; Animals; Basal Metabolism; Blood Glucose; Calorimetry, Indirect; Carbon Dioxide; Dietary Fats; Energy Metabolism; Fatty Acids, Unsaturated; Linoleic Acid; Lipid Peroxidation; Male; Metabolic Syndrome; Oleic Acid; Oxygen Consumption; Rats; Rats, Wistar; Risk Factors; Stearic Acids; Triglycerides; Tumor Necrosis Factor-alpha

We examined relationships between visceral fat amount and alterations in serum fatty acid composition, both of which represent critical factors in the development of metabolic syndrome.. Correlations were analyzed between visceral fat thickness as measured by ultrasonography and proportions of individual fatty acids in 21 normal-weight and 24 overweight Japanese men.. Significant associations were identified in overweight subjects. Visceral fat thickness displayed positive correlations to levels of palmitic acid and saturated fatty acids (r=0.475, P<0.05 and r=0.545, P<0.01, respectively); and negative correlations to levels of linoleic acid and polyunsaturated fatty acids (r=-0.513, P<0.05 and r=-0.428, P<0.05, respectively). Visceral fat thickness was also correlated with estimated desaturase activities, with positive correlations to Delta9- and Delta6-desaturase activities and negative correlations to Delta5-desaturase activity (r=0.580, P<0.01, r=0.669, P<0.01 and r=-0.559, P<0.01, respectively). No significant associations were identified in normal-weight subjects.. Significant associations between visceral fat amount and alterations in serum fatty acid composition were identified, but only in overweight individuals.

Topics: Adiposity; Adult; Aged; Alcohol Drinking; Body Mass Index; Chromatography, Gas; Diabetes Mellitus; Fatty Acids; Fatty Acids, Unsaturated; Flame Ionization; Humans; Hypertension; Japan; Linoleic Acid; Linoleoyl-CoA Desaturase; Male; Metabolic Syndrome; Middle Aged; Overweight; Palmitic Acid; Smoking; Ultrasonography; Waist Circumference

Feeding stroke-prone spontaneously hypertensive rats (SHRSP) a diet rich in fructose results in a profound glucose intolerance not observed in the normotensive Wistar Kyoto (WKY) strain. The aim of this study was to investigate the role of the liver in the underlying mechanisms in the SHRSP.. SHRSP and WKY rats were fed either 60% fructose or regular chow for 2 weeks with blood pressure being measured using tail-cuff plethysmography and radiotelemetry. Intraperitoneal glucose tolerance tests were performed and livers harvested for analysis of expression of inflammatory mediators and antioxidant proteins by western blotting and quantitative reverse transcriptase-PCR. The serum triglyceride content and fatty acid profiles were also measured.. Feeding SHRSP and WKY on 60% fructose for 2 weeks resulted in glucose intolerance with no increases in levels of blood pressure. Serum triglycerides were increased in both strains of fructose-fed rats with the highest levels being observed in the SHRSP. The serum fatty acid profiles were changed with large increases in the amounts of oleic acid (18.1) and reductions in linoleic acid (18.2). Levels of expression of c-jun N-terminal kinase/stress activated protein kinase (JNK/SAPK), and nuclear factor kappaB (NF-kappaB) were shown to be unchanged between the livers of the chow and fructose-fed groups. In contrast, protein levels of the three isoforms of superoxide dismutase (SOD) were upregulated in liver of SHRSP fed on fructose while only manganese SOD (MnSOD) was upregulated in fructose-fed WKY rats.. These results demonstrate that the major contribution of the liver in the early pathogenesis of metabolic syndrome may be an increased secretion of triglyceride containing altered proportions of fatty acid pools. Feeding rats a diet rich in fructose does not affect hepatic expression of inflammatory pathways and the increased hepatic SOD expression may constitute an early protective mechanism.

Topics: Animals; Blood Pressure; Dietary Carbohydrates; Fructose; Glucose Intolerance; Hypertension; JNK Mitogen-Activated Protein Kinases; Linoleic Acid; Liver; Male; Metabolic Syndrome; Mitogen-Activated Protein Kinase 8; NF-kappa B; Oleic Acid; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Superoxide Dismutase; Triglycerides

A specific fatty acid (FA) composition in plasma lipid esters is related to the metabolic syndrome (MetS) and may influence the development of the MetS.. The objective was to define and study FA factors as measures of dietary fat quality and endogenous FA metabolism in relation to MetS.. Principal factor analysis was performed to define specific FA factors in men participating in a population-based cohort study-the Uppsala Longitudinal Study of Adult Men. The factors were generated at ages 50 (n = 2009) and 70 (n = 576) y, and relations between FA factors and MetS (National Cholesterol Education Program) were studied in cross-sectional and prospective (20 y) analyses.. The factor analysis generated 3 major FA factors: a low-linoleic acid (LA) factor, a dietary saturated FA factor, and an n-3 polyunsaturated FA (PUFA) factor. All factors differed between those subjects with MetS (n = 281 of 2009) and those without MetS at age 50 y; only the low-LA factor differed at age 70 y, which suggests an association between MetS and fat quality. The low-LA factor (odds ratio: 1.51; 95% CI: 1.28, 1.79; P < 0.0001) and the n-3 PUFA factor (0.76; 0.64, 0.90; P < 0.001) predicted MetS development over 20 y, independent of smoking habits, physical activity, and BMI.. The generated FA factors, which presumably represent dietary fat quality and endogenous FA metabolism, may be important in the development of MetS. This finding supports current dietary recommendations to increase PUFA intakes and restrict saturated FA intakes.

Topics: Aged; Cholesterol Esters; Cohort Studies; Cross-Sectional Studies; Dietary Fats; Factor Analysis, Statistical; Fatty Acids; Fatty Acids, Omega-3; Humans; Linoleic Acid; Lipid Metabolism; Longitudinal Studies; Male; Metabolic Syndrome; Middle Aged; Predictive Value of Tests; Prospective Studies; Stearoyl-CoA Desaturase; Sweden

There is a multitude of data showing that coronary heart disease is affected by the quality of dietary fat. The fatty acid composition of serum lipids has been shown to reflect that of the diet. It is likely that, after myocardial infarction, both the health-care professionals and the patients themselves pay more attention to dietary guidelines. In order to assess the correctness of this assumption, we compared the composition of serum fatty acids in 40 male subjects with a history of myocardial infarction (MI) with that of 40 age-matched controls, both from the FINRISK study. The percentage composition of fatty acids of total serum lipids was analysed by gas chromatography. In comparison with the control group, the MI group had higher body mass index (BMI), a higher prevalence of diabetes, higher level of serum triglycerides and a lower level of serum high-density lipoprotein (HDL) cholesterol, all indicators of the metabolic syndrome. The MI group had higher proportions of serum palmitic (16:0) and oleic acids (18:1), and a lower proportion of linoleic (18:2 n-6) acid than the control group. The metabolic syndrome is accompanied by an elevated level of serum insulin, which is known to enhance the synthesis of saturated and monounsaturated fatty acids, such as 16:0 and 18:1, and to stimulate the activity delta-6 desaturase, decreasing the concentration of linoleic acid. Our results suggest that the observed serum fatty acid composition in subjects with coronary heart disease is dependent on metabolic factors in addition to dietary fatty acid composition.

Topics: Aged; Body Mass Index; Cholesterol, HDL; Cross-Sectional Studies; Diabetes Mellitus, Type 2; Dietary Fats; Fatty Acids; Finland; Humans; Linoleic Acid; Male; Metabolic Syndrome; Middle Aged; Myocardial Infarction; Oleic Acid; Palmitic Acid; Triglycerides