Plasma Lipids in Human Linoleic Acid Deficiency

Collins, F. D.; Sinclair, Andrew J.; Royle, Jenny; Coats, D. A.; Maynard, Andy; Leonard, R. F.

doi:10.1159/000175332

Cited by 192 publications

(53 citation statements)

References 13 publications

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“…These isomers have been shown to occur in EFA-deficient rats (22 (2,8). This is the established biochemical indication of a metabolic deficiency state which has been repeatedly found characteristic of EFA deficiency (2,8,(12)(13)(14)(15). Under normal circumstances, the body converts linoleic acid (which cannot be biosynthesized) to arachidonic acid.…”

Section: Discussionmentioning

confidence: 97%

The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally.

Wene¹,

Connor²,

DenBesten³

1975

J. Clin. Invest.

200

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A B S T R A C T The hypothesis that clinical and biochemical essential fatty acid deficiency (EFA) might occur from the feeding of eucaloric, fat-free diets was tested in two experiments in healthy men. In Study I, eight men were given fat-free, eucaloric diets containing 80% of calories as glucose and 20% as amino acid hydrolysates by a constant drip over a 24-h period. The diets were fed in succession for periods of 2 wk each, either through a superior vena cava catheter or via a nasogastric tube. EFA deficiency was detected by decreases in linoleic acid and by the appearance of 5, 8.11-eicosatrienoic acid in lipid fractions of plasma. Linoleic acid decreased significantly during 2 wk of the fat-free diet given intravenously from 48.8 to 9.8% (percent of total fatty acids) in cholesterol esters, from 21.2 to 3.2% in phospholipids, from 9.6 to 2.0% in free fatty acids, and from 14.1 to 2.6% in triglycerides. Eicosatrienoic acid, normally undetectable, appeared 0.6% in cholesterol esters, 2.5% in phospholipids, 0.2% in free fatty acids, and 2.3% in triglycerides. EFA deficiency occurred similarly during the nasogastric feeding.In Study II a subject received the same diet continuously by the nasogastric route for 10 days followed by a 24-h fast. He was then given the fat-free diet intermittently in three meals per day for 3 days. Finally. he was repleted with a diet containing 2.6% linoleic acid. By the 3rd day of the continuous nasogastric feeding, linoleic acid had fallen significantly and eicosatrienoic acid had appeared in plasma lipid fractions as in Study I. These findings were accentuated by day 10. Adipose tissue fatty acid composition did not change. Free fatty

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Section: Discussionmentioning

confidence: 97%

The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally.

Wene¹,

Connor²,

DenBesten³

1975

J. Clin. Invest.

200

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“…The most concentrated eicosanoid detected was 5-HETE, which had a concentration of 0.0019 ± 0.00001 nmol/g of brain in the n-6 PUFAadequate rats and 0.0013 ± 0.000007 nmol/g of brain in In rats, the level of LA at which tissue ARA concentrations plateau is 1,200 mg of LA per 100 g of diet, and this intake is considered the recommended minimum LA intake ( 25 ). This level is comparable to the recommended level of LA for humans: 1,000-1,500 mg of LA per 100 g of food, which equates to ‫ف‬ 2-3% of energy (42)(43)(44). However, more recent studies suggest that these are overestimations of the actual LA requirement, and there is a concern that the amount of LA in the average human diet is too high ( 45 ).…”

Section: Discussionmentioning

confidence: 99%

Chronic dietary n-6 PUFA deprivation leads to conservation of arachidonic acid and more rapid loss of DHA in rat brain phospholipids

Lin

Chen

Hildebrand

et al. 2015

Journal of Lipid Research

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This article is available online at http://www.jlr.org disease, Parkinson's disease, bipolar disorder, and major depression ( 7-9 ).ARA and DHA can either be obtained directly from the diet or synthesized from their nutritionally essential precursor fatty acids linoleic acid (18:2n-6; LA) and ␣ -linolenic acid (18:3n-3; ALA) respectively, which are the main dietary n-6 and n-3 PUFAs. Thus, it is of interest to determine whether changes in the level of dietary n-6 or n-3 PUFAs can alter the concentrations of ARA and/or DHA in the brain, and more importantly, whether these dietary changes affect their metabolism. In fact, clinical trials in humans are underway, with the assumption that lowering n-6 PUFAs may decrease brain ARA and its metabolism ( 1 ).Several studies have investigated the effects of dietary n-3 PUFA deprivation on brain ARA and DHA concentrations and metabolism in rats. Feeding rats an n-3 PUFAdeprived diet that contains ALA at a concentration of 0.04% versus an n-3 PUFA-adequate diet containing ALA at 4.4% of all fatty acids decreased the concentration of DHA by 37% and increased docosapentaenoic acid (DPA) n-6 concentration by 95% in brain total phospholipids, but did not change the concentration of ARA ( 10 ). This study also reported that n-3 PUFA deprivation conserves DHA in rat brain phospholipids extending the half-life from 33 to 90 days. This conservation response was selective for DHA, as n-3 PUFA deprivation did not alter the half-life or rate of ARA metabolic consumption ( 11 ). Alterations in brain DHA concentration and metabolism appear to occur below a threshold of 0.8% ALA in the diet, Abstract To determine how the level of dietary n-6 PUFA affects the rate of loss of arachidonic acid (ARA) and DHA in brain phospholipids, male rats were fed either a deprived or adequate n-6 PUFA diet for 15 weeks postweaning, and then subjected to an intracerebroventricular infusion of 3 H-ARA or 3 H-DHA. Brains were collected at fi xed times over 128 days to determine half-lives and the rates of loss from brain phospholipids ( J out ). Compared with the adequate n-6 PUFA rats, the deprived n-6-PUFA rats had a 15% lower concentration of ARA and an 18% higher concentration of DHA in their brain total phospholipids. Loss half-lives of ARA in brain total phospholipids and fractions (except phosphatidylserine) were longer in the deprived n-6 PUFA rats, whereas the J out was decreased. In the deprived versus adequate n-6 PUFA rats, the J out of DHA was higher. In conclusion, chronic n-6 PUFA deprivation decreases the rate of loss of ARA and increases the rate of loss of DHA in brain phospholipids. Thus, a low n-6 PUFA diet can be used to target brain ARA and DHA metabolism. The brain is specifi cally enriched with the two PUFAs arachidonic acid (20:4n-6; ARA) and DHA (22:6n-3), which are considered important for normal brain function. Bioactive mediators from ARA and DHA, the eicosanoids and docosanoids, respectively, regulate many processes including neuroinfl ammation, pain perception, and blood fl ow...

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“…In any case, the increase in plasma cholesterol was temporary (25), regressing within 2 wk of discontinuing infusion, and was not associated with any untoward side effects. On the other side of the picture, lipid infusions have been found to be necessary to avoid essential fatty acid deficiency (26,40,41) and development of fatty liver (26,42,43), a recognized complication of the glucose system. Furthermore in patients receiving intravenous feeding at home (now observed for up to 5 yr) (26,42,43) no untoward reaction to Intralipid has been noted with daily infusions given over several years.…”

Section: Protocol Imentioning

confidence: 99%

Metabolic studies in total parenteral nutrition with lipid in man. Comparison with glucose.

Hoy¹,

Anderson²,

Nakhooda³

et al. 1976

J. Clin. Invest.

283

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A B S T R A C T A study was undertaken of patients on a regimen of total parenteral nutrition comparing the nitrogen balance, energy substrates, blood amino acids, immunoreactive insulin, and immunoreactive glucagon levels during the sequential infusion of nonprotein calories as either glucose alone (glucose system) or 83% as Intralipid (Pharmacia Fine Chemicals, Montreal, Canada) and 17% glucose (lipid system). These nonprotein calories were administered with a constant background of amino acids (1 g/kg per day), vitamins, and minerals. Each system was infused for a week at a time and the order of infusion randomized. In some patients whole blood arteriovenous (A-V) levels of amino acids were measured across forearm muscle.During the glucose system there was a significantly higher level of pyruvate, lactate, alanine, and immunoreactive insulin, consistent with glucose being the principal source of energy. In contrast, during the lipid system there was a rise in free fatty acids and ketone bodies with a fall in insulin, suggesting that lipid was now the principal source of energy. Despite these two very diverse metabolic situations the nitrogen balance with both systems was positive to a comparable degree after the establishment of equilibrium. Correspondingly, A-V differences of whole blood amino acid nitrogen showed uptake by muscle to an equivalent degree with both systems.Clinical studies indicated that the lipid system as defined herein could be infused by peripheral vein for up to This work was presented in part at the Symposium on

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Plasma Lipids in Human Linoleic Acid Deficiency

Cited by 192 publications

References 13 publications

The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally.

The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally.

Chronic dietary n-6 PUFA deprivation leads to conservation of arachidonic acid and more rapid loss of DHA in rat brain phospholipids

Metabolic studies in total parenteral nutrition with lipid in man. Comparison with glucose.

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