PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “FATTY ACIDS, ESSENTIAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 127 records · Page 7Linked to original sources
PubMed1992

Non-eicosanoid functions of essential fatty acids: regulation of adenosine-related functions in cultured neuroblastoma cells.

Studies have demonstrated that augmenting the omega 6 polyunsaturated-fatty-acid (PUFA) content of N1E-115 neuroblastoma cells by media supplementation with linoleic acid results in greater than or equal to 2-fold increases in basal levels of intracellular cyclic AMP (cAMP). Data suggested some involvement of increased production of adenosine from endogenous metabolites; however, increases in adenosine were not related to increased activity of 5'-nucleotidase or decreased uptake of extracellular adenosine. PUFA-dependent elevations in basal cAMP were evident within 1 min of exposure to a phosphodiesterase inhibitor; this phenomenon did not appear to be due to PUFA-dependent changes in Ca2+ uptake or to increases in sensitivity of adenylate cyclase to Ca2+. Forskolin-stimulated cAMP formation was 3-fold higher in PUFA-enriched cells than in control cells, which suggested a direct effect on the functioning of the catalytic unit. Linoleic acid supplementation resulted in a 2-fold increase in the maximum amounts of cAMP produced in response to the stable adenosine analogue, 5'-N'ethylcarboxy-amidoadenosine (NECA). The altered stimulatory response did not involve eicosanoid formation, but may have been related to an increase in the number of stimulatory adenosine receptors, as judged by binding of [3H]NECA. These studies indicate that membrane PUFA modulate adenosine-related functions in neuroblastoma cells, and suggest that a complex series of mechanisms is involved in this regulation.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1998

The metabolism and n-6/n-3 ratio of essential fatty acids in rats: effect of dietary arachidonic acid and a mixture of sesame lignans (sesamin and episesamin).

In this study, we examined the effect of dietary arachidonic acid (AA) and sesame lignans on the content and n-6/n-3 ratio of polyunsaturated fatty acid (PUFA) in rat liver and the concentrations of triglyceride (TG) and ketone bodies in serum. For 4 wk, rats were fed two types of dietary oils: (i) the control oil diet groups (CO and COS): soybean oil/perilla oil = 5:1, and (ii) the AA-rich oil group (AO and AOS): AA ethyl esters/palm oil/perilla oil = 2:2:1, with (COS and AOS) or without (CO and AO) 0.5% (w/w) of sesame lignans. Dietary AA and sesame lignans significantly affected hepatic PUFA metabolism. AA content and n-6/n-3 ratio in the liver were significantly increased in the AO group, despite the dietary total of n-6 PUFA being the same in all groups, while AOS diet reduced AA content and n-6/n-3 ratio to a level similar to the CO and COS groups. These results suggest that (i) dietary AA considerably affects the hepatic profile and n-6/n-3 ratio of PUFA, and (ii) dietary sesame lignans reduce AA content and n-6/n-3 ratio in the liver. In the AO group, the concentration of acetoacetate was significantly increased, but the ratio of beta-hydroxybutyrate/acetoacetate was decreased. On the other hand, the AO diet increased the concentration of TG in serum by almost twofold as compared to other groups. However, the AOS diet significantly reduced serum TG level as compared to the AO group. In addition, the AOS diet significantly increased the acetoacetate level, but reduced the beta-hydroxybutyrate/acetoacetate ratio. These results suggest that dietary sesame lignans promote ketogenesis and reduce PUFA esterification into TG. This study resulted in two findings: (i) sesame lignans inhibited extreme changes of the n-6/n-3 ratio by reducing hepatic PUFA content, and (ii) the reduction of hepatic PUFA content may have occurred because of the effects of sesame lignans on PUFA degradation (oxidation) and esterification.

Animals↗
PubMed1985

Essential fatty acids in diabetes and systemic lupus erythematosus (SLE) patients.

Sera obtained from normal subjects and juvenile-onset diabetes (JD) and systemic lupus erythromatus (SLE) patients were examined for free fatty acid composition and 6-keto-PGF1 alpha content. In addition, prostaglandins in urine samples from normal and diabetic individuals were separated by HPLC, and 6-keto-PGF1 alpha levels were monitored by RIA. Arachidonate (20:4) content in diabetic and SLE individuals were significantly lower than that of controls. Urine from diabetic individuals showed decreased levels of 6-keto-PG F1 alpha. The study also indicated that RIA measurements on crude biological samples may yield erroneous data due to immune cross reactivity with other compounds.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

The reversibility of cancer: the relevance of cyclic AMP, calcium, essential fatty acids and prostaglandin E1.

Transformed cells in culture can be normalised (made to undergo reverse transformation) by exposure to cyclic AMP, prostaglandin (PG) E1 and certain drugs. One of these drugs, thioproline, has been successfully used in treating human cancer. All cancer cells have a number of common characteristics: they exhibit aerobic glycolysis, they fail to show feedback regulation of cholesterol biosynthesis, they do not regulate cytoplasmic calcium levels normally and they produce excessive amounts of 2 series PGs. It has been known since 1975 that transformed cells cannot make PGE1 because of loss of the delta-6-desaturase enzyme which converts linoleic acid to gamma-linolenic acid. There is evidence that PGE1 acting in concert with thromboxane A2 has effects which make it able to reverse all the metabolic abnormalities common to all cancer cells. It is therefore argued that loss of the ability to make PGE1 and/or thromboxane A2 may be the critical step in malignant change in many forms of cancer. Restoration of normal PGE1 synthesis by providing gamma-linolenic or dihomogammal inolenic acids which will by-pass the blocked desaturase, whould be of value in normalising malignant cells and reversing cancer growth. Since this approach is completely non-toxic it is here seriously suggested that it might be used as a first step in treatment of those cancers where current evidence suggests that delay in the administration of orthodox treatment is unlikely to affect prognosis.

Animals↗