Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LINOLEIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,135 records · Page 63Linked to original sources
PubMed1993

Correlation between histopathology and linoleic acid levels in five meningioma types.

The total fatty acid compositions of neoplastic tissues in 5 different meningioma types (meningotheliomatous, transitional, vascular, fibroblastic, atypical), analysed by gas-liquid chromatography, are presented in correlation with their histopathology. The benign meningioma types (first 3) had higher relative percentages of linoleic acid, compared to the apparently malignant meningioma types (fibroblastic, atypical). From these results it is suggested that a high relative percentage of linoleic acid is characteristic of benign neoplastic growth, while a low relative percentage may correlate with increased malignancy.

Biomarkers↗
PubMed1981

Dietary linoleic acid and salt-induced hypertension.

Male Wistar rats chronically fed a low level (0.41%) of linoleic acid (LA) in the diet as supplied by 5% olive oil developed a significant elevation of systolic blood pressure as compared with rats fed either a medium (4.2%) or high (9.4%) level of dietary LA. Chronic excess intake of NaCl (3.75% in the diet) was associated with a significant elevation of blood pressure on all three diets but a low level of LA in the diet exaggerated the salt-induced hypertension. The results suggest that inadequate dietary LA may result in an increase in systolic blood pressure regardless of the sodium content of the diet.

Animals↗
PubMed2002

Trans-10, cis-12 conjugated linoleic acid increases fatty acid oxidation in 3T3-L1 preadipocytes.

The purpose of this study was to examine the effect of 0-50 micromol/L trans-10, cis-12 conjugated linoleic acid (CLA) and cis-9, trans-11 CLA isomers on lipid and glucose metabolism in cultures of differentiating 3T3-L1 preadipocytes. Specifically, we investigated the effects of 6 d of CLA treatment on the following: 1) (14)C-glucose and (14)C-oleic acid incorporation and esterification into lipid; 2) (14)C-glucose and (14)C-fatty acid oxidation; and 3) basal and isoproterenol-stimulated lipolysis. Trans-10, cis-12 CLA supplementation (25 and 50 micromol/L) increased both (14)C-glucose and (14)C-oleic acid incorporation into the cellular lipid fraction, which was primarily triglyceride (TG), compared with bovine serum albumin (BSA) controls. Although glucose oxidation ((14)C-glucose to (14)C-CO(2)) was unaffected by CLA supplementation, oleic acid oxidation ((14)C-oleic acid to (14)C-CO(2)) was increased by approximately 55% in the presence of 50 micromol/L trans-10, cis-12 CLA compared with BSA controls. In contrast, 50 micromol/L linoleic acid (LA) and cis-9, trans-11 CLA-treated cultures had approximately 50% lower CO(2) production from (14)C-oleic acid compared with control cultures after 6 d of fatty acid exposure. Finally, 50 micromol/L trans-10, cis-12 CLA modestly increased basal, but not isoproterenol-stimulated lipolysis compared with control cultures. Thus, the TG-lowering actions of trans-10, cis-12 CLA in cultures of 3T3-L1 preadipocytes may be via increased fatty acid oxidation, which exceeded its stimulatory effects on glucose and oleic acid incorporation into lipid.

3T3 Cells↗
PubMed1986

The effect of orally administered secondary autoxidation products of linoleic acid on the activity of detoxifying enzymes in the rat liver.

Radioactive secondary autoxidation products of linoleic acid were administered orally to rats and the incorporation of radioactive substances into lipids was investigated in the liver. The radioactive substances were significantly incorporated into hepatic mitochondrial and microsomal lipids 12 h after the administration. 80% of the radioactivity in mitochondria was detected in neutral lipids. The radioactivity in microsomal neutral lipids significantly decreased and the activity in phospholipids increased 12 h after the administration. On the other hand, contents of lipid peroxide and thiobarbituric acid reactive substances in liver were significantly increased by 40% at 15 h after the administration of the secondary autoxidation products. Activity of marker enzymes used for an indication of the hepatic injury was also elevated. Glutathione peroxidase activity increased 3-fold and catalase activity increased 1.5-fold. Activity of mitochondrial NAD-dependent aldehyde dehydrogenase, however, was decreased by 50%. It seems likely that the secondary autoxidation products orally administered are detoxified in the hepatic mitochondria, metabolized to neutral lipids, and further metabolized to phospholipids in microsomes, while as the incorporated secondary autoxidation products induces hepatic injury by lipid peroxidation.

Administration, Oral↗
PubMed1997

Effect of monochlorohydrins of linoleic acid on guinea-pig cardiac papillary muscles.

The hydrogen peroxide (H2O2)-myeloperoxidase system can convert linoleic acid (LA) to monochlorohydrins. LA monochlorohydrins can also be produced when LA monoepoxides are subjected to low pH solutions. We chemically synthesized and purified LA monochlorohydrins and examined their effect on the developed tension of guinea-pig papillary muscles in vitro in terms of both concentration and the duration of exposure. A decrease in muscular tension was observed immediately after addition of LA monochlorohydrins at concentrations of 30, 100, and 300 microM. We also compared the effect of LA monochlorohydrins on muscle tension with those of LA monoepoxides.

Animals↗
PubMed1999

Dietary linoleic acid, immune inhibition and disease.

Review of the evidence available in published literature supports a radical change in viewpoint with respect to disease in countries where maize is the predominant dietary component. In these countries, the pattern of disease is largely determined by a change in immune profile caused by metabolites of dietary linoleic acid. High intake of linoleic acid in a diet deficient in other polyunsaturated fatty acids and in riboflavin results in high tissue production of prostaglandin E2, which in turn causes inhibition of the proliferation and cytokine production of Th1 cells, mediators of cellular immunity. Tuberculosis, measles, hepatoma, secondary infection in HIV and kwashiorkor are all favoured by this reduction in cellular immunity. Diet-associated inhibition of the Th1 subset is a major contributor to the high prevalence of these diseases found in areas of sub-Saharan Africa where maize is the staple.

Africa↗
PubMed2000

Linoleic acid conjugation by human intestinal microorganisms is inhibited by glucose and other substrates in vitro and in gnotobiotic rats.

The anticarcinogen conjugated linoleic acid (CLA) is a product of bacterial activity that isomerizes linoleic acid (LA) in the rumen of herbivores. Therefore, fatty dairy products in the human diet are enriched with CLA. Although bacteria capable of in vitro LA conjugation were detected in the human intestinal tract, CLA synthesis from dietary sunflower seed oil was not observed in gnotobiotic rats associated with these intestinal bacteria. The objective of the study was to investigate variables that affect LA conjugation. In vitro, LA conjugation was strongly inhibited by glucose and other substrates. Concentrations of 1.5 mmol glucose/L inhibited LA conjugation by 50%. Methyl-alpha-D-glucoside was a less effective inhibitor than glucose, and 2-deoxy-D-glucose did not inhibit LA conjugation at all. To analyze the concentration of carbohydrates in intestinal contents, the LA-conjugating bacterial mixed culture and human fecal microorganisms were introduced into germ-free rats. Samples of feces and cecum and colon contents of both groups exhibited in vitro LA-conjugating activity. Rats associated with human intestinal microorganisms contained 5.7 +/- 1. 3 mmol glucose/L in the cecal contents and 6.6 +/- 1.0 mmol glucose/L in the colonic contents. Rats associated with CLA-producing bacterial culture contained 3.4 +/- 1.3 mmol glucose/L in the cecal contents and 4.2 +/- 1.0 mmol glucose/L in the colonic contents. These values are within a range that may explain the observed inhibition of LA conjugation in vivo.

Animals↗
PubMed2004

Insulin resistance-associated cardiovascular disease: potential benefits of conjugated linoleic acid.

Type 2 diabetes and associated cardiovascular disease have reached global epidemic proportions. Recent data from the World Health Organization Multinational Study of Vascular Disease in Diabetes indicate that cardiovascular disease is the leading cause of mortality (52% of deaths) in individuals with type 2 diabetes. Although insulin resistance plays a critical role in the pathogenesis of type 2 diabetes-related cardiovascular disease, other related risk factors often cluster in a single patient; the combination of insulin resistance and these risk factors is known as the metabolic syndrome. According to the World Health Organization definition, this constellation of risk factors includes hypertension, elevated plasma triacylglycerol, reduced HDL cholesterol, central obesity, and microalbuminuria. The Multiple Risk Factor Intervention Trial showed that, although diabetes or insulin resistance is an independent risk factor for cardiovascular disease mortality, these other components of the metabolic syndrome confer additive risk. Thus, to effectively address cardiovascular disease in persons with diabetes, intervention would ideally target all these factors. Conjugated linoleic acid could represent a candidate agent. The therapeutic potential of conjugated linoleic acid against insulin resistance-associated cardiovascular disease is discussed on the basis of the reported effects of conjugated linoleic acid on individual components of the metabolic syndrome.

Albuminuria↗
PubMedDate not supplied

Conjugated linoleic acid (CLA) inhibits growth of Caco-2 colon cancer cells: possible mediation by oleamide.

We have previously observed that dietary conjugated linoleic acid (CLA) inhibited colon tumorigenesis induced by 1,2-dimethylhydrazine in rats. The present study was performed to determine the mechanisms by which CLA inhibits colon cancer cell growth. CLA markedly inhibited Caco-2 cell growth, while linoleic acid (LA) slightly increased growth. Both CLA and LA increased the production of material reactive to antibodies against prostaglandin (PG)E2 and leukotriene (LT)B4, estimated by a competitive enzyme immunoassays (EIA), in a dose-dependent manner. However, the magnitude of the increase was markedly higher with CLA than that with LA, suggesting that this material was not PGE2 or LTB4. The active compound was isolated by thin-layer chromatography and the nuclear magnetic resonance and infrared spectra revealed that the structure was identical to that of oleamide. The purified oleamide inhibited cell growth and cross-reacted with the EIA. These results indicate that inhibition of Caco-2 cell growth by CLA may be due in part to increased oleamide production.

Caco-2 Cells↗
PubMed2001

[Effects of conjugated linoleic acid on the metastasis of mouse melanoma B16-MB].

In order to explore the effects of conjugated linoleic acid on tumor metastasis, the proliferation, gap junction intercellular communication (GJIC), adhesion to extracellular matrix, and metastasis cascades of tumor cells were imitated in cell culture. The results showed that 100 and 200 mumol/L conjugated linoleic acid could inhibit the proliferation and the adhesion of tumor cells to extracellular matrix, and could recover its gap junction intercellulor communication.

Animals↗
PubMed1985

Difference in susceptibility to injury by linoleic acid hydroperoxide between endothelial and smooth muscle cells of arteries.

Electron microscopic examination of the effect of linoleic acid hydroperoxide on cultured smooth muscle cells from human umbilical artery revealed that incubation of the cells with 5.0 nmol/ml (in terms of malondialdehyde) of the hydroperoxide for 3 h caused a decrease in the electron density of the mitochondrial matrix and that dilatation of the rough-surfaced endoplasmic reticulum occurred when the cells were incubated with 10 nmol/ml of the hydroperoxide. These concentrations are higher by one order of magnitude than those required for the same effects on cultured endothelial cells from human umbilical vein. A similar difference in susceptibility to injury by linoleic acid hydroperoxide was found between cultured endothelial and smooth muscle cells from fetal calf aorta. The effects of the hydroperoxide on the respiration of these cells paralleled the observed morphological changes.

Animals↗
PubMed2006

Conjugated linoleic acid reduces phorbol ester-induced prostaglandin F2alpha production by bovine endometrial cells.

Recent interest in conjugated linoleic acid (CLA) research stems from the well-documented anticarcinogenic, antiatherogenic, antidiabetic, and antiobesity properties of CLA in animal models. The objective of this study was to examine the effects of 2 CLA isomers (cis-9,trans-11 and trans-10,cis-12) on phorbol 12,13-dibutyrate (PDBu)-induced PGF2alpha production in cultured bovine endometrial (BEND) cells. Confluent BEND cells were incubated in the absence (control) or presence of 100 microM each of linoleic acid, cis-9,trans-11 CLA, or trans-10,cis-12 CLA for 24 h. After incubation, cells were rinsed and then stimulated with PDBu (100 ng/mL) for 6 h. Compared with untreated cells, PDBu stimulated PGF2alpha secretion (+25-fold) within 6 h. The increases in PGF(2alpha) secretion were paralleled by signifi-cant induction of prostaglandin endoperoxide synthase-2 (PGHS-2) mRNA (+63-fold) and protein (+1.6-fold) expression. In spite of stimulatory effects on PGHS-2 and peroxisome proliferator-activated receptor delta (PPARdelta) mRNA responses, CLA greatly decreased PGF2alpha production by PDBu-stimulated BEND cells. There was no evidence for PDBu or CLA modulation of PPARdelta protein synthesis in cultured BEND cells. Results indicated that CLA modulation of PGF2alpha production by BEND cells was not mediated through PGHS-2 or PPARdelta gene repression.

Animals↗
PubMed1990

Incorporation and effects of dietary eicosapentaenoate (20:5(n-3)) on plasma and erythrocyte lipids of the marmoset following dietary supplementation with differing levels of linoleic acid.

The effect of dietary eicosapentaenoic acid (EPA, 20:5(n-3), as the ethyl ester) on plasma lipid levels and the incorporation of EPA into erythrocyte and plasma lipids were investigated in the marmoset monkey. Marmosets were fed high mixed-fat diets (14.5% total fat) supplemented with or without 0.8% EPA for 30 weeks. Markedly elevated plasma cholesterol (16.4 mmol/l) was induced by an atherogenic-type diet but with EPA supplementation, plasma cholesterol increased to only 6.6 mmol/l. Plasma triacylglycerol levels were not elevated with an atherogenic type diet. Substantial EPA incorporation was evident for plasma phospholipid, triacylglycerol and cholesterol ester fractions. The proportion of docosapentaenoic acid (22:5(n-3)) but not docosahexaenoic acid (22:6(n-3)) was also elevated in these plasma lipid fractions. Greatest incorporation of EPA occurred when it was administered with an atherogenic type diet having a P:M:S (polyunsaturated:monounsaturated:saturated) fatty acid ratio of about 0.2:0.6:1.0 in comparison to the control diet of 1.0:1.0:1.0. Incorporation of EPA and 22:5(n-3)) into erythrocyte phospholipids was also apparent and this was at the expense of linoleic acid (18:2(n-6)). These results in the marmoset highlight both the cholesterol-lowering properties of EPA and the extent of its incorporation into plasma lipids and erythrocyte membrane phospholipids with far greater incorporation occurring when the level of dietary linoleic acid was reduced.

Animals↗
PubMed2002

Combined effects of dietary conjugated linoleic acid and sesamin triacylglycerol and ketone body production in rat liver.

The effects of a combination of dietary conjugated linoleic acid (CLA) supplemented with sesamin on hepatic ketogenesis and triacylglycerol secretion were compared using the livers of rats fed diets containing 1% CLA or linoleic acid (LA) in combination with 0.2% sesamin for 14 d, respectively. The feeding of CLA, as compared to LA, caused a significant reduction in the weight of perirenal adipose tissue but not that of epididymal adipose tissue, and affected neither growth parameters nor hepatic lipid concentration. Hepatic production of ketone bodies was consistently higher in rats fed CLA than in those fed LA, while triacylglycerol secretion was reversed. No significant difference was noted in the hepatic secretion of cholesterol among the groups. Although there was no effect of the dietary combination of CLA with sesamin on adipose tissue weight, hepatic lipid parameters and ketone body production were observed: i.e., triacylglycerol secretion tended to be reduced. These results suggest that the dietary combination of CLA with sesamin may be an effective approach for lowering serum triacylglycerol levels. The decreased hepatic secretion of triacylglycerol is, in part, due to enhanced fatty acid oxidation in the liver.

Animals↗
PubMed2003

Adenoma growth stimulation by the trans-10, cis-12 isomer of conjugated linoleic acid (CLA) is associated with changes in mucosal NF-kappaB and cyclin D1 protein levels in the Min mouse.

Conjugated linoleic acid (CLA) is a term used to describe the different conjugated isomers of linoleic acid. CLA has been found to be anticarcinogenic in mammary cancer, but its effects on colon carcinogenesis are still inconclusive. In this study, the isomer-specific effects of the cis-9, trans-11 and trans-10, cis-12 CLA isomers were investigated in the Min mouse model for intestinal carcinogenesis. The Min mice (n = 10/group) were fed either an AIN-93G control diet or a diet containing 1 g/100 g cis-9, trans-11 or trans-10, cis-12 CLA for 8 wk. The number and size of adenomas were measured and the proteins from the small intestinal tissues extracted for immunoblotting analysis. The number of adenomas did not differ, but the size of the adenomas was greater in the distal part of the small intestine in mice fed the trans-10, cis-12 isomer than in controls (1.19 +/- 0.16 vs. 0.94 +/- 0.21 mm, mean +/- SD, P < 0.01). The same isomer caused an increase in lipid peroxidation, measured as urinary 8-iso-prostaglandin (PG)F(2alpha). Nuclear p65 protein of the mucosal tissue was not detectable in the trans-10, cis-12 group, which differed (P < 0.05) from the control group. Cyclin D1, a target for the nuclear factor (NF)-kappaB pathway, was elevated in the trans-10, cis-12 group compared with the control group (P < 0.01), but cyclooxygenase-2 levels were not higher. There was no difference in beta-catenin protein levels between the groups. The results indicate that the trans-10, cis-12 isomer of CLA can act as a cancer promoter in colon carcinogenesis possibly through pathways affecting NF-kappaB and cyclin D1.

Adenoma↗
PubMed2003

Production responses of dairy cows to dietary supplementation with conjugated linoleic acid (CLA) during the transition period and early lactation.

Holstein cows (n = 30) entering second or greater lactation were fed fat supplements (90 g/d of fatty acids) consisting of Ca salts of either palm fatty acid distillate (control) or a mixture of palm fatty acid distillate and mixed isomers of conjugated linoleic acid (CLA, 30.4 g/ d) from 2 wk prepartum through 20 wk postpartum to determine whether CLA would inhibit milk fat synthesis during early lactation and, in turn, affect energy metabolism of dairy cows during the transition period and early lactation. Feeding CLA did not affect DMI or plasma concentrations of glucose, nonesterfied fatty acids, or beta-hydroxbutyrate during the prepartum period and did not affect postpartum DMI. Feeding CLA reduced milk fat content by 12.5% during early lactation; however, cows fed CLA tended to produce approximately 3 kg/d more milk during the first 20 wk of lactation. Feeding CLA tended to decrease the contribution of short- and medium-chain (C < or = 16) fatty acids to milk fat. Changes in milk yield, milk fat content, and milk fatty acid composition were not apparent until after the second week of lactation. Yield of 3.5% fat-corrected milk, milk protein content, milk protein composition, and calculated energy balance were not affected by treatment. Postpartum concentrations of glucose, nonesterfied fatty acids, and beta-hydroxbutyrate in plasma and hepatic content of glycogen and triglycerides were similar between treatments. These data imply that with CLA treatment in early lactation, dairy cows decreased milk fat synthesis and appeared to respond by partitioning more nutrients toward milk synthesis rather than improving net energy balance.

3-Hydroxybutyric Acid↗
PubMed1977

Involvement of cytochrome b5 in the oxidative desaturation of linoleic acid to gamma-linolenic acid in rat liver microsomes.

The effects of antibodies against microsomal electron-transport components on the in vitro activity of delta6-desaturation of linoleic acid to gamma-linolenic acid have been studied in intact microsomal membranes of rat liver. Reduced nicotinamide adenine dinucleotide (NADH) or reduced nicotinamide adenine dinucleotide phosphate (NADPH) (0.87 mM) served as electron donors, and effectively prompted the delta6-desaturase activities with yields of about 1.1 to 1.3 nmol per mg of protein in 10 min. Of the two antibodies studied under the same in vitro conditions, i.e., rabbit antisera preparations against rat liver microsomal hydrophilic parts of cytochrome b5 and NADPH-cytochrome c reductase, only the antibody against cytochrome b5 demonstrated a marked ability to inhibit the delta6-desaturase activity. This evidence supports a participation of cytochrome b5 in the delta6-desaturation of linoleic acid and suggests a pathway analogous to the delta9-desaturation of stearyl-CoA.

Animals↗