Effect of degree of unsaturation in dietary fatty acids on arachidonic acid mobilization by peritoneal macrophages

Lipids ◽  
1996 ◽  
Vol 31 (6) ◽  
pp. 661-666 ◽  
Author(s):  
María T. Mitjavila ◽  
María C. Rodríguez ◽  
María P. Sáiz ◽  
Sergio Lloret ◽  
Juan J. Moreno
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Peritoneal Macrophages ◽  
Dietary Fatty Acids ◽  
Degree Of Unsaturation

scholarly journals Effect of fatty acid chain length and saturation on the gastrointestinal handling and metabolic disposal of dietary fatty acids in women

1999 ◽  
Vol 81 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Amanda E. Jones ◽  
Michael Stolinski ◽  
Ruth D. Smith ◽  
Jane L. Murphy ◽  
Stephen A. Wootton
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Stearic Acid ◽  
Palmitic Acid ◽  
Chain Length ◽  
Time Course ◽  
Absorbed Dose ◽  
Dietary Fatty Acids ◽  
Fatty Acid Chain ◽  
Degree Of Unsaturation

The gastrointestinal handling and metabolic disposal of [1-13C]palmitic acid, [1-13C]stearic acid and [1-13C]oleic acid administered within a lipid–casein–glucose–sucrose emulsion were examined in normal healthy women by determining both the amount and nature of the13C label in stool and label excreted on breath as13CO2. The greatest excretion of13C label in stool was in the stearic acid trial (9.2 % of administered dose) whilst comparatively little label was observed in stool in either the palmitic acid (1.2 % of administered dose) or oleic acid (1.9 % of administered dose) trials. In both the palmitic acid and oleic acid trials, all of the label in stool was identified as being present in the form in which it was administered (i.e. [13C]palmitic acid in the palmitic acid trial and [13C]oleic acid in the oleic acid trial). In contrast, only 87 % of the label in the stool in the stearic acid trial was identified as [13C]stearic acid, the remainder was identified as [13C]palmitic acid which may reflect chain shortening of [1-13C]stearic acid within the gastrointestinal tract. Small, but statistically significant, differences were observed in the time course of recovery of13C label on breath over the initial 9 h of the study period (oleic acid = palmitic acid > stearic acid). However, when calculated over the 24 h study period, the recovery of the label as13CO2was similar in all three trials (approximately 25 % of absorbed dose). These results support the view that chain length and degree of unsaturation may influence the gastrointestinal handling and immediate metabolic disposal of these fatty acids even when presented within an emulsion.

Functional analysis of rat liver citrate carrier promoter: differential responsiveness to polyunsaturated fatty acids

2008 ◽  
Vol 417 (2) ◽  
pp. 561-571 ◽  
Author(s):  
Fabrizio Damiano ◽  
Gabriele V. Gnoni ◽  
Luisa Siculella
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Docosahexaenoic Acid ◽  
Polyunsaturated Fatty Acids ◽  
Dietary Fatty Acids ◽  
Luciferase Reporter ◽  
H4iie Cells ◽  
E Box ◽  
Citrate Carrier ◽  
Response Region

CiC (citrate carrier), a mitochondrial membrane protein, plays an important metabolic role by transporting acetyl-CoA into the cytosol for fatty acid and cholesterol synthesis. Several studies showed that CiC activity and expression is regulated by dietary fatty acids. In the present study we report data on the structural and functional characterization of the 5′-flanking region of the rat Cic gene. By transient transfection assays in H4IIE rat hepatoma cells, a PUFA (polyunsaturated fatty acids) response region has been identified within the CiC promoter. A cluster of putative binding sites for several transcription factors, composed of a NF-Y (nuclear factor-Y) site, an E-box-like site, a SRE1 (sterol regulatory element 1)-like site and four Sp1 (stimulatory protein 1) sites, was localized in the promoter region. Luciferase reporter gene and gel mobility shift assays indicated that a functional E-box-like, essential to the basal CiC promoter activity, confers responsiveness to activation by SREBP (SRE-binding protein)-1c. This study provides evidence for SREBP-1c as a principal target for PUFA regulation of CiC transcription. In H4IIE cells, overexpression of nSREBP (nuclear SREBP)-1c over-rides arachidonic acid (C20:4, n-6) suppression, but does not prevent the repression by docosahexaenoic acid (C22:6, n-3). ChIP (chromatin immunoprecipitation) assays in H4IIE cells showed that docosahexaenoic acid affects the binding of NF-Y, Sp1 and SREBP-1 to the PUFA response region of CiC promoter, whereas arachidonic acid alters only the binding of SREBP-1. Our data show that PUFA inhibition of hepatic Cic gene transcription is mediated not only by the nuclear level of SREBP-1c, but also might involve a reduction in Sp1 and NF-Y DNA binding, suggesting differential mechanisms in the Cic gene regulation by different PUFA.

Effects of Dietary Fatty Acids on Platelet Aggregation and Platelet Thromboxane B2 Production in the Rabbit.

1979 ◽  
Author(s):  
E. Agradi ◽  
E. Tremoli ◽  
A. Petroni ◽  
C. Colombo ◽  
C. Galli
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Corn Oil ◽  
Dietary Fatty Acids ◽  
Thromboxane B2 ◽  
The Difference ◽  
Isocaloric Diets ◽  
Dietary Treatments ◽  
Induced Aggregation

Semisynthetic isocaloric diets containing 25% of either butter or corn oil were fed to male rabbits for periods of 21 days and 2½ months. Platelet aggregation induced by threshold concentrations of collagen and sodium arachidonate and the conversion of labelled arachidonic acid were then studied. Response of platelets from butter-fed animals was considerably higher to arachidonate, whereas the thresholds for collagen-induced aggregation were similar in both groups of animals. Conversion of labelled arachidonic acid to thromboxane B2, studied at different substrate concentrations in washed platelets, was significantly higher, at low substrate concentration, at 21 days in the butter fed group, and the difference was still present after 2½ months of treatment. Conversion of arachidonic acid to the hydroxy fatty acids by lipoxygenase activity was not affected by the dietary treatments. In conclusion, the metabolic conversion of exogenous arachidonic acid to thromboxane B2 appears to be selectively affected by the type of dietary fatty acids and this effect is associated with changes in the response of platelets to aggregating concentrations of arachidonic acid.

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