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Results for “FATTY ACIDS, ESSENTIAL”

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PubMed1988

Changes in human plasma essential fatty acid levels as a result of administration of linoleic acid and gamma-linolenic acid.

Administration of doses of linoleic acid (LA) up to 36 g/d in humans raised blood levels of linoleic acid but not of its metabolites. This is probably because the conversion of LA to gamma-linolenic acid (GLA) is slow and rate-limiting. We have found that administration of relatively small amounts of GLA, up to 360 mg/d, raises human blood levels of dihomogammalinolenic acid (DGLA) and arachidonic acid (AA).

Adult↗
PubMed1985

[Biochemistry and significance of prostaglandins, prostacyclins, thromboxanes and leukotrienes and the modification of their biosynthesis by essential fatty acids].

A survey is given of the biochemistry and importance of the prostaglandins, the thromboxanes, the prostacyclins and the leukotrienes. The formation of these compounds takes place from poly-unsaturated fatty acids and is regulated: here the phospholipase A2 plays a role. Among others the prostaglandins take part in the regulation of the blood supply of various tissues (heart, kidneys), in the regulation of the reproduction and in the evokation of labour. The thromboxanes and prostacyclins influence the aggregation and the desaggregation of the thrombocytes, respectively. The leukotrienes take part in the regulation of the permeability of the capillaries, in the migration of the leucocytes, the formation of inflammatory processes and in the evokation of asthma bronchiale. The insufficient intake leads to functional disturbances in various tissues, which partly are to be traced back to a decrease of the formation of the tissue hormones mentioned. An intake transgressing the demand has a favourable effect in various diseases: thus the inclination to aggregation of the thrombocytes is decreased and the development of arteriosclerotic changes is inhibited.

Animals↗
PubMed1986

Metabolism of essential fatty acids by human epidermal enzyme preparations: evidence of chain elongation.

The present studies were undertaken in order to delineate the source of human epidermal arachidonic acid, 20:4(n-6). Epidermal microsomal preparations from normal (N) and diseased epidermis (clinically uninvolved (PU) and involved psoriatic (PI) epidermis) were incubated in vitro with either [14C]18:2(n-6), [14C]20:3(n-6) or [14C]malonyl CoA to determine the activities of the delta 6, delta 5 desaturases and elongate, respectively. Experiments were performed in parallel with rat liver microsomal preparations where enzyme activities are well documented. Data derived from the enzymatic assays were compared to fatty acid composition data derived from epidermal total lipids. The enzymatic conversion rates were determined after methylation and separation of the 14C-labeled fatty acid methyl esters by argentation thin-layer chromatography and reverse phase high-performance liquid chromatography. Our data demonstrated: that N, PU, and PI epidermis were all capable of elongating 18:3(n-6) into 14C-labeled 20:3(n-6) via the addition of [14C]malonyl CoA, and this activity was markedly elevated (fivefold) in PI preparations; that N, PU, and PI epidermal preparations lacked the capacity to desaturate 18:2(n-6) and 20:3(n-6); and striking alterations in the individual fatty acids (as weight percent) in the total fatty acids of the PI epidermal extracts when compared to the PU and N extracts. These findings indicate that epidermal arachidonic acid is not biosynthesized locally from tissue linoleic acid and must, therefore, depend on contribution from another endogenous source.

Acetyltransferases↗