ABSTRACT
INTRODUCTION: During adolescence, dairy product intake has shown conflicting associations with metabolic syndrome (MetS) components, which are risk factors for cardiovascular disease (CVD). This study aims to investigate the association between plasma fatty acids (FAs) C15:0, C17:0, and t-C16:1n-7, as biomarkers of dairy intake, with MetS and its components in Mexican adolescents. METHODS: A sample of 311 participants from the Early Life Exposure in Mexico City to Environmental Toxicants (ELEMENT) cohort was included in this cross-sectional analysis. FA concentrations were measured in plasma as a percentage of total FA. We used quantile regression models stratified by sex to evaluate the association between FA quantiles and MetS components, adjusting for age, socioeconomic status (SES), sedentary behavior, BMI z-score, pubertal status, and energy intake. RESULTS: We found significant associations between dairy biomarkers and the median of MetS variables. In females, t-C16:1n-7 was associated with a decrease of 2.97 cm in WC (Q4 vs. Q1; 95% CI: -5.79, -0.16). In males, C15:0 was associated with an increase of 5.84 mm/Hg in SBP (Q4 vs. Q1; CI: 1.82, 9.85). For HDL-C, we observed opposite associations by sex. C15:0 in males was associated with decreased HDL-C (Q3 vs. Q1: ß = -4.23; 95% CI: -7.98, -0.48), while in females, C15:0 and t-C16:1n-7 were associated with increased HDL-C (Q3 vs. Q1: ß = 4.75; 95% CI: 0.68, 8.82 and Q4 vs. Q1: ß = 6.54; 95% CI: 2.01, 11.07), respectively. Additionally, in both sexes, different levels of C15:0, C17:0, and t-C16:1n-7 were associated with increased triglycerides (TG). CONCLUSION: Our results suggest that adolescent dairy intake may be associated in different directions with MetS components and that associations are sex-dependent.
Subject(s)
Fatty Acids , Metabolic Syndrome , Male , Female , Humans , Adolescent , Metabolic Syndrome/epidemiology , Cross-Sectional Studies , Mexico/epidemiology , Dietary Fats , Dairy Products/analysis , Risk Factors , BiomarkersABSTRACT
BACKGROUND: Metabolic disorders such as obesity and type 2 diabetes (T2D) coincide with an increased expression of pro-inflammatory factors. The NLRP3 inflammasome is a complex that activates the pro-inflammatory cytokine IL-1ß. (NOD-like receptor protein 3). Some nutrients, such as fatty acids, influence inflammatory processes. For example, in clinical studies, higher trans-palmitoyl acid (TP) concentrations coincide with lower adiposity and lower risk of developing T2D. This study aims to evaluate the effect of TP on NLRP3 expression in a rodent model of diet-induced obesity (DIO). METHODS: C57BL/6J mice were fed ad libitum with a control or a high-fat diet (HFD), added with or without TP (3 g/kg diet), for 11 weeks. IL-1ß was quantified in serum, and NLRP3-related gene expression was explored in epididymal adipose tissue. RESULTS: Despite increased weight gain in both high-fat groups, the high-fat TP group gained less weight than the high-fat group. In addition, NLRP3 and caspase-1 expression was higher in the HFD groups, but no differences were observed between the HFD and the HFD TP groups. Serum IL-1ß levels were not different among groups. CONCLUSIONS: Diet supplementation with TP prevents weight gain and has a neutral influence over NLRP3 expression and IL-1ß concentration in a DIO mice model.
INTRODUCCIÓN: Las alteraciones metabólicas como la obesidad y diabetes tipo 2 (DT2) coinciden con la expresión aumentada de factores proinflamatorios. Un complejo que induce la activación de la citocina proinflamatoria IL-1ß es el inflamasoma NLRP3 (NOD-like receptor protein 3). Algunos nutrimentos, como los ácidos grasos, influencian los procesos inflamatorios. Por ejemplo, en estudios clínicos, mayores concentraciones del ácido trans-palmitoléico (TP) coinciden con una menor adiposidad y un menor riesgo de desarrollar DT2. El objetivo de este estudio fue evaluar el efecto del TP sobre la expresión del inflamasoma NLRP3 en un modelo de obesidad inducida por dieta (OID) en roedores. MÉTODOS: Se alimentaron ratones C57BL/6J ad libitum con una dieta control o alta en lípidos (AL), adicionada o no con TP (3 g/kg dieta), durante 11 semanas. Se cuantificó la concentración de IL-1ß en elsuero de los animales, y en el tejido adiposo epididimal se midió la expresión de los componentes del inflamasoma. RESULTADOS: A pesar del aumento de peso en ambos grupos de dieta con alto contenido en lípidos, el grupo alto en lípidos TP ganó menos peso que el grupo AL. Por otro lado, la expresión de genes del inflamasoma resultó mayor en los grupos AL, pero no se encontraron diferencias entre los grupos AL y AL TP. Además, no se observaron diferencias en la concentración de IL-1ß en suero entre grupos. CONCLUSIONES: La dieta suplementada con TP previno el aumento del peso corporal, pero no modificó la expresión de los componentes del inflamasoma ni la concentración de IL-1ß en suero.
Subject(s)
Diabetes Mellitus, Type 2 , Inflammasomes , Mice , Animals , Humans , Inflammasomes/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein/genetics , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Rodentia/metabolism , Mice, Inbred C57BL , Obesity/etiology , Diet, High-Fat/adverse effects , Weight GainABSTRACT
Abstract Background: Metabolic disorders such as obesity and type 2 diabetes (T2D) coincide with an increased expression of pro-inflammatory factors. The NLRP3 inflammasome is a complex that activates the pro-inflammatory cytokine IL-1β. (NOD-like receptor protein 3). Some nutrients, such as fatty acids, influence inflammatory processes. For example, in clinical studies, higher trans-palmitoyl acid (TP) concentrations coincide with lower adiposity and lower risk of developing T2D. This study aims to evaluate the effect of TP on NLRP3 expression in a rodent model of diet-induced obesity (DIO). Methods: C57BL/6J mice were fed ad libitum with a control or a high-fat diet (HFD), added with or without TP (3 g/kg diet), for 11 weeks. IL-1β was quantified in serum, and NLRP3-related gene expression was explored in epididymal adipose tissue. Results: Despite increased weight gain in both high-fat groups, the high-fat TP group gained less weight than the high-fat group. In addition, NLRP3 and caspase-1 expression was higher in the HFD groups, but no differences were observed between the HFD and the HFD TP groups. Serum IL-1β levels were not different among groups. Conclusions: Diet supplementation with TP prevents weight gain and has a neutral influence over NLRP3 expression and IL-1β concentration in a DIO mice model.
Resumen Introducción: Las alteraciones metabólicas como la obesidad y diabetes tipo 2 (DT2) coinciden con la expresión aumentada de factores proinflamatorios. Un complejo que induce la activación de la citocina proinflamatoria IL-1β es el inflamasoma NLRP3 (NOD-like receptor protein 3). Algunos nutrimentos, como los ácidos grasos, influencian los procesos inflamatorios. Por ejemplo, en estudios clínicos, mayores concentraciones del ácido trans-palmitoléico (TP) coinciden con una menor adiposidad y un menor riesgo de desarrollar DT2. El objetivo de este estudio fue evaluar el efecto del TP sobre la expresión del inflamasoma NLRP3 en un modelo de obesidad inducida por dieta (OID) en roedores. Métodos: Se alimentaron ratones C57BL/6J ad libitum con una dieta control o alta en lípidos (AL), adicionada o no con TP (3 g/kg dieta), durante 11 semanas. Se cuantificó la concentración de IL-1β en elsuero de los animales, y en el tejido adiposo epididimal se midió la expresión de los componentes del inflamasoma. Resultados: A pesar del aumento de peso en ambos grupos de dieta con alto contenido en lípidos, el grupo alto en lípidos TP ganó menos peso que el grupo AL. Por otro lado, la expresión de genes del inflamasoma resultó mayor en los grupos AL, pero no se encontraron diferencias entre los grupos AL y AL TP. Además, no se observaron diferencias en la concentración de IL-1β en suero entre grupos. Conclusiones: La dieta suplementada con TP previno el aumento del peso corporal, pero no modificó la expresión de los componentes del inflamasoma ni la concentración de IL-1β en suero.
ABSTRACT
The burden of disease associated with acne vulgaris has continued to increase over time in the world population. This continued growth suggests that there is an unmet dermatologic need for this condition worldwide. Potential sequelae of acne, such as scarring, depigmentation, and marked emotional and psychological problems (e.g., low self-esteem), can lead to significant morbidity. The purpose of this study was to investigate whether dietary supplementation with magnesium, phosphate, omega 6 (linoleic acid calcium salt - C18:2 fatty acid Ca salt), and omega 7 (palmitoleic acid calcium salt - C16:1 fatty acid Ca salt) would help patients with acne vulgaris, and to compare with isotretinoin (13-cis retinoic acid). Magnesium has anti-inflammatory properties. Linoleic and palmitoleic acids have bactericidal activity against Staphylococcus aureus and Cutibacterium acnes (formerly known as Propionibacterium acnes). A single-blind randomized study was conducted in which 257 patients were treated with the above dietary supplementation (group A) and 275 patients with isotretinoin (group B) for 6 months. All patients in group A (100%) reported complete regression of symptoms after 6 months of treatment. On the other hand, 187 subjects (68%) in group B reported complete resolution of symptoms during the same period. The difference between the groups (p < 0.05) was statistically significant. The study was approved by the CEP/CONEP. This natural formulation promotes regression and/or cure of acne vulgaris symptoms and has better results than drugs (such as isotretinoin), without significant side effects.
Subject(s)
Acne Vulgaris , Isotretinoin , Adolescent , Humans , Acne Vulgaris/drug therapy , Calcium , Dietary Supplements , Fatty Acids/therapeutic use , Isotretinoin/therapeutic use , Magnesium , Phosphates , Single-Blind MethodABSTRACT
Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High-Fat diet, added with or without TP (3 g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high-fat diet, reduced visceral adipose tissue weight and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.
Subject(s)
Adiposity , Lipolysis , Adipose Tissue/metabolism , Animals , Diet, High-Fat/adverse effects , Fatty Acids, Monounsaturated , Mice , Mice, Inbred C57BL , Obesity/metabolism , RodentiaABSTRACT
Brazil nut oil is mostly composed of unsaturated fatty acids, some of which are associated with decreased incidence of cardiovascular diseases. Vegetable proteins have been increasingly used as wall material for partial replacement of carbohydrates and whey proteins. In order to create an oil preservation method, Brazil nut oil was encapsulated with three different types of vegetable protein concentrates and gum arabic (GA): rice (RPC + GA); pea (PPC + GA); and soy (SPC + GA) .For this purpose, vegetable protein concentrates were characterized, and after the drying process the physicochemical characteristics of the microparticles were evaluated. The most stable emulsion, after seven days of evaluation, was composed of RPC + GA. RPC + GA. This treatment was also more stable based on the shelf life assessments. We concluded that RCP microparticles were the best option for encapsulating Brazil nut oil in comparison with the other particles evaluated. In addition, the product obtained is potentially capable of being included in various processed foods.
Subject(s)
Bertholletia , Fatty Acids, Unsaturated , Gum Arabic , Oxidation-Reduction , Plant Proteins, DietaryABSTRACT
Palmitoleic acid (POA, 16:1n-7) is a lipokine that has potential nutraceutical use to treat non-alcoholic fatty liver disease. We tested the effects of POA supplementation (daily oral gavage, 300 mg/Kg, 15 days) on murine liver inflammation induced by a high fat diet (HFD, 59% fat, 12 weeks). In HFD-fed mice, POA supplementation reduced serum insulin and improved insulin tolerance compared with oleic acid (OA, 300 mg/Kg). The livers of POA-treated mice exhibited less steatosis and inflammation than those of OA-treated mice with lower inflammatory cytokine levels and reduced toll-like receptor 4 protein content. The anti-inflammatory effects of POA in the liver were accompanied by a reduction in liver macrophages (LM, CD11c+; F4/80+; CD86+), an effect that could be triggered by peroxisome proliferator activated receptor (PPAR)-γ, a lipogenic transcription factor upregulated in livers of POA-treated mice. We also used HFD-fed mice with selective deletion of PPAR-γ in myeloid cells (PPAR-γ KOLyzCre+) to test whether the beneficial anti-inflammatory effects of POA are dependent on macrophages PPAR-γ. POA-mediated improvement of insulin tolerance was tightly dependent on myeloid PPAR-γ, while POA anti-inflammatory actions including the reduction in liver inflammatory cytokines were preserved in mice bearing myeloid cells deficient in PPAR-γ. This overlapped with increased CD206+ (M2a) cells and downregulation of CD86+ and CD11c+ liver macrophages. Moreover, POA supplementation increased hepatic AMPK activity and decreased expression of the fatty acid binding scavenger receptor, CD36. We conclude that POA controls liver inflammation triggered by fat accumulation through induction of M2a macrophages independently of myeloid cell PPAR-γ.
Subject(s)
Fatty Acids, Monounsaturated/pharmacology , Inflammation/drug therapy , Non-alcoholic Fatty Liver Disease/drug therapy , PPAR gamma/genetics , AMP-Activated Protein Kinase Kinases , Animals , B7-2 Antigen/genetics , CD11c Antigen/genetics , Diet, High-Fat/adverse effects , Fatty Acids, Monounsaturated/metabolism , Humans , Inflammation/genetics , Inflammation/metabolism , Inflammation/pathology , Insulin Resistance/genetics , Lectins, C-Type/genetics , Liver/drug effects , Liver/metabolism , Liver/pathology , Mannose Receptor , Mannose-Binding Lectins/genetics , Mice , Myeloid Cells/drug effects , Myeloid Cells/metabolism , Non-alcoholic Fatty Liver Disease/genetics , Non-alcoholic Fatty Liver Disease/metabolism , Oleic Acid/metabolism , Oleic Acid/pharmacology , Protein Kinases/genetics , Receptors, Cell Surface/geneticsABSTRACT
BACKGROUND AND AIMS: Animal models have shown that adipose-derived palmitoleic acid may act as a lipokine by conferring resistance to diet-induced obesity; however, human epidemiologic studies investigating this relationship thus far have not provided data in support of this hypothesis. Because metabolic syndrome and cardiovascular disease are intricately linked with the former being a major risk factor for the latter, we hypothesized that adipose-derived palmitoleic acid may be inversely associated with myocardial infarction. We examined whether adipose tissue palmitoleic acid was associated with nonfatal acute myocardial infarction in a representative population of Costa Rican adults. METHODS AND RESULTS: Odds ratios of nonfatal acute myocardial infarction by quintiles of adipose tissue palmitoleic acid were calculated using conditional logistic regression in a case-control study of 1828 cases and 1828 controls matched by age, sex, and area of residence. We observed an inverse relationship between nonfatal acute myocardial infarction and adipose tissue palmitoleic acid (OR for highest quintile compared to lowest quintile of palmitoleic acid: 0.55; 95% CI: 0.41, 0.75; P for trend: <0.0001). We additionally observed a significant positive association between adipose tissue palmitoleic acid and high-density lipoprotein cholesterol. CONCLUSION: These data demonstrate an inverse association between adipose tissue palmitoleic acid and nonfatal acute myocardial infarction; however, further research is required in order to better understand the opposing associations between palmitoleic acid and high-density lipoprotein cholesterol and systolic blood pressure.
Subject(s)
Adipose Tissue/chemistry , Fatty Acids, Monounsaturated/analysis , Myocardial Infarction/epidemiology , Myocardial Infarction/metabolism , Aged , Biomarkers/analysis , Case-Control Studies , Costa Rica/epidemiology , Down-Regulation , Female , Humans , Male , Middle Aged , Myocardial Infarction/diagnosis , Risk Assessment , Risk FactorsABSTRACT
SCOPE: Fatty acids (FAs) may affect endothelial cell (EC) function, influencing atherogenesis and inflammatory processes. Palmitoleic acid (POA) has been described as an anti-inflammatory FA. However, its effects on ECs are underexplored. This study compares the effects of POA with those of palmitic acid (PA) and oleic acid (OA) on EC inflammatory responses. METHODS AND RESULTS: EAHy926 cells (EC lineage) are exposed to PA, OA, or POA, and stimulated with tumor necrosis factor (TNF)-α. Associated with the FA's own incorporation, PA induces a twofold increase in arachidonic acid, while POA increases the amount of cis-vaccenic acid. PA, but not OA, enhances the production of IL-6 and IL-8 in response to TNF-α. In contrast, POA decreases production of monocyte chemotactic protein (MCP)-1, IL-6, and IL-8 compared to PA. TNF-α increases surface intercellular adhesion molecule-1 expression previously decreased by POA. TNF-α stimulation increases the expression of NFκB, cyclooxygenase (COX)-2, MCP-1, and IL-6 genes and reduces the expression of peroxisome proliferator-activated receptor (PPAR)-α gene. PA enhances the expression of MCP-1, IL-6, and COX-2 genes, while POA downregulates these genes, decreases expression of NFκB, and upregulates PPAR-α gene expression. CONCLUSION: POA has anti-inflammatory effects on ECs stimulated with TNF-α and may counter endothelial dysfunction.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Endothelial Cells/drug effects , Fatty Acids, Monounsaturated/pharmacology , Oleic Acid/pharmacology , Palmitic Acids/pharmacology , Cell Line , Cell Survival/drug effects , Chemokine CCL2/genetics , Chemokine CCL2/metabolism , Chemokine CCL5/genetics , Chemokine CCL5/metabolism , Fatty Acids, Monounsaturated/pharmacokinetics , Gene Expression Regulation , Human Umbilical Vein Endothelial Cells , Humans , Inflammation/drug therapy , Inflammation/genetics , Inflammation/metabolism , Intercellular Adhesion Molecule-1/metabolism , Interleukin-6/genetics , Interleukin-6/metabolism , Oleic Acid/pharmacokinetics , Palmitic Acids/pharmacokinetics , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Although dietary fatty acids can modulate metabolic and immune responses, the effects of palmitoleic acid (16:1n-7) remain unclear. Since this monounsaturated fatty acid is described as a lipokine, studies with cell culture and rodent models have suggested it enhances whole body insulin sensitivity, stimulates insulin secretion by ß cells, increases hepatic fatty acid oxidation, improves the blood lipid profile, and alters macrophage differentiation. However, human studies report elevated blood levels of palmitoleic acid in people with obesity and metabolic syndrome. These findings might be reflection of the level or activity of stearoyl-CoA desaturase-1, which synthesizes palmitoleate and is enhanced in liver and adipose tissue of obese patients. The aim of this review is to describe the immune-metabolic effects of palmitoleic acid observed in cell culture, animal models, and humans to answer the question of whether palmitoleic acid is a plausible nonpharmacological strategy to prevent, control, or ameliorate chronic metabolic and inflammatory disorders. Despite the beneficial effects observed in cell culture and in animal studies, there are insufficient human intervention studies to fully understand the physiological effects of palmitoleic acid. Therefore, more human-based research is needed to identify whether palmitoleic acid meets the promising therapeutic potential suggested by the preclinical research.
Subject(s)
Fatty Acids, Monounsaturated/therapeutic use , Metabolic Syndrome/drug therapy , Obesity/drug therapy , Acetyltransferases/physiology , Animals , Atherosclerosis/drug therapy , Atherosclerosis/prevention & control , Cholesterol, LDL/blood , Fatty Acid Elongases , Humans , Insulin Resistance , Metabolic Syndrome/prevention & control , Obesity/prevention & control , Stearoyl-CoA Desaturase/physiologyABSTRACT
Obesity is a metabolic, multifactorial disease that is underpinned by factors such as genetics, epigenetics, as well as high-energy food intake and sedentarism. Obesity is often associated with, and exacerbated by, other metabolic disorders such as type 2 diabetes mellitus (T2DM). A hallmark of T2DM is failure of insulin secretion from pancreatic ß-cell to regulate blood glucose disposal into peripheral tissues, such as skeletal muscle, termed insulin resistance, as well as deregulation of pancreatic α-cell function. It has been proposed that insulin resistance is, in part, a consequence of impaired signal transduction of insulin caused by several molecules released from adipose tissue that include (adipo)cytokines and fatty acids. However, not all fatty acids exert a negative impact on insulin sensitivity. In fact, it has been suggested that palmitoleic acid (16:1n-7) has hormone-like properties and improves some metabolic parameters that are impaired in obesity and T2DM. Moreover, in vitro approaches reveal that cis-16:1n-7 can influence pancreatic ß-cell survival, insulin secretion, and skeletal muscle insulin response and adipocyte metabolism. In vivo experiments using animal models show that the ingestion of cis-16:1n-7 or sources of it (e.g., macadamia oil) can partially prevent the metabolic alterations caused by high-fat/carbohydrate diets. In general, studies in humans found positive associations between higher trans-16:1n-7 proportion in plasma phospholipids and improved insulin sensitivity or decreased the onset of T2DM. However, plasma cis-16:1n-7 data are still controversial. In this brief review, we discuss the main studies on 16:1n-7 effects on obesity and T2DM and their potential for clinical application.
Subject(s)
Diabetes Mellitus, Type 2/diet therapy , Fatty Acids, Monounsaturated/administration & dosage , Glucose/metabolism , Obesity/metabolism , Animals , Fatty Acids, Monounsaturated/pharmacology , Homeostasis/drug effects , Humans , Insulin Resistance , Insulin-Secreting Cells/metabolism , Obesity/complications , Phospholipids/bloodABSTRACT
The objective of this research was to investigate the genotoxic potential of the oil of H. annuus L. (sunflower) seeds via the Ames test as well as its oxidative properties and lipid composition. The pre-incubation method, system metabolic activation (S9 fraction) and five S. typhimurium strains (TA97, TA98, TA100, TA1535 and TA102) were employed for the Ames test. The oxidative stability and fatty acid composition were analyzed by standard methods and gas chromatography. A revertant analysis showed no significant differences between the treatment doses (10-200 µl/plate) and the negative controls, regardless of S9+ and S9-, and included all of the S. typhimurium strains. Chromatographic analysis showed high levels of polyunsaturated fatty acids, followed by monounsaturated, saturated and total trans-isomers. Among the polyunsaturated, monounsaturated and saturated fatty acids, linoleic, oleic and palmitic acids predominated. The results suggest that the sunflower oil is not genotoxic as indicated by frameshift mutations and base pair substitutions regardless of the treatment dose, but shows dose-dependent toxicity. The oxidative properties of the sunflower oil were consistent with the requirements of national and international standards. However, its composition could also indicate phytotherapeutic properties.
ABSTRACT
Palmitic acid is a negative regulator of insulin activity. At the molecular level, palmitic acid reduces insulin stimulated Akt Ser473 phosphorylation. Interestingly, we have found that incubation with palmitic acid of human umbilical vein endothelial cells induced a biphasic effect, an initial transient elevation followed by a sustained reduction of SERCA pump protein levels. However, palmitic acid produced a sustained inhibition of SERCA pump ATPase activity. Insulin resistance state appeared before there was a significant reduction of SERCA2 expression. The mechanism by which palmitic acid impairs insulin signaling may involve endoplasmic reticulum stress, because this fatty acid induced activation of both PERK, an ER stress marker, and JNK, a kinase associated with insulin resistance. None of these effects were observed by incubating HUVEC-CS cells with palmitoleic acid. Importantly, SERCA2 overexpression decreased the palmitic acid-induced insulin resistance state. All these results suggest that SERCA pump might be the target of palmitic acid to induce the insulin resistance state in a human vascular endothelial cell line. Importantly, these data suggest that HUVEC-CS cells respond to palmitic acid-exposure with a compensatory overexpression of SERCA pump within the first hour, which eventually fades out and insulin resistance prevails.
Subject(s)
Endoplasmic Reticulum Stress/drug effects , Endothelial Cells/drug effects , Fatty Acids, Monounsaturated/pharmacology , Insulin Resistance/physiology , Palmitic Acid/pharmacology , Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism , Apoptosis/drug effects , Cell Line , Endoplasmic Reticulum/metabolism , Endothelial Cells/metabolism , HumansABSTRACT
The ethyl acetate extract from the fruit pulp of Caryocar coriaceum Wittm (Caryocaraceae), popularly known as pequi, has wide applications in popular medicine. Preclinical tests have demonstrated the therapeutic properties of the oil. We investigated the antinociceptive and anti-inflammatory effects of Pequi C. coriaceum Wittm ethyl acetate extract (PCCO) on zymosan-induced arthritis in rat knee joint. The animals were pretreated with PCCO for 7 consecutive days or with a single dose. Paw elevation time (PET), leukocyte infiltration, myeloperoxidase activity (MPO) and cytokine levels were assessed 4h after zymosan injection. Synovial tissue was harvested for immunohistochemical analysis, edema and vascular permeability. We observed a significant decrease in PET with PCCO pretreatment. PCCO showed a significant reduction of leukocyte migration and a decrease in MPO. Decreases were observed in cytokine release in the synovial fluid and TNF-α and cyclooxygenase-1 immunostaining in synovial tissue. Edema was inhibited by treatment with all doses of PCCO. The data suggest that PCCO exerts antinociceptive and anti-inflammatory effects on arthritis in rats.
Subject(s)
Analgesics/pharmacology , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Arthritis, Experimental/drug therapy , Ericales/chemistry , Fruit/chemistry , Plant Extracts/chemistry , Plant Extracts/pharmacology , Analgesics/isolation & purification , Animals , Anti-Inflammatory Agents, Non-Steroidal/isolation & purification , Arthritis, Experimental/chemically induced , Arthritis, Experimental/pathology , Cyclooxygenase 1/metabolism , Cytokines/metabolism , Edema/chemically induced , Edema/drug therapy , Edema/pathology , Joints/pathology , Male , Neutrophil Infiltration/drug effects , Peroxidase/metabolism , Rats , Rats, Wistar , Synovial Fluid/drug effects , Synovial Fluid/metabolism , Tumor Necrosis Factor-alpha/metabolism , ZymosanABSTRACT
BACKGROUND: Purified palmitoleic acid (16-1; omega-7) has shown lipid-lowering and anti-inflammatory benefits in open label, epidemiologic, and animal studies. OBJECTIVE: Our objective was to perform the first randomized controlled trial of purified palmitoleic acid supplementation in humans. METHODS: Adults with dyslipidemia and evidence of mild systemic inflammation (high-sensitivity C-reactive protein [hs-CRP] between 2 and 5 mg/L) were randomly allocated to receive either 220.5 mg of cis-palmitoleic acid (n = 30) or an identical capsule with placebo (1000 mg of medium chain triglycerides, n = 30) once per day for 30 days. Participants were asked to maintain their current diet. Serum lipids and hs-CRP were drawn at baseline and study completion. RESULTS: At 30 days, there were significant mean (95% confidence interval [CI]) reductions in CRP (-1.9 [-2.3 to -1.4] mg/L), triglyceride (-30.2 [-40.2 to -25.3] mg/dL), and low-density lipoprotein (LDL) (-8.9 [-12.0 to -5.8] mg/dL), and a significant increase in high-density lipoprotein (HDL) (2.4 [1.5, 3.3] mg/dL) in the intervention group compared with control. These changes equated to 44%, 15%, and 8% reductions in CRP, triglyceride, and LDL respectively, and a 5% increase in HDL compared with control. CONCLUSIONS: Purified palmitoleic acid may be useful in the treatment of hypertriglyceridemia with the beneficial added effects of decreasing LDL and hs-CRP and raising HDL. Further study is needed to elucidate mechanisms and establish appropriate human doses.