Effects of dietary α‐linolenic acid on the conversion and oxidation of<sup>13</sup>C‐α‐linolenic acid

Vermunt, Susanne H. F.; Mensink, Ronald P.; Simonis, M. M. G.; Hornstra, Gerard

doi:10.1007/bf02664762

Cited by 126 publications

(106 citation statements)

References 24 publications

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“…However, amounts of 13 C18X2n-6 and its 13 C labelled LCPs varied considerably between the subjects. In a recent similar study with 13 C a-linolenic acid (Vermunt et al, 2000), we found a signi®cant negative correlation between plasma 13 C LCPs and the 13 C elimination with breath CO 2 . In the present study, in the three subjects of whom 13 C elimination was known, the subject with the highest amounts of 13 C LCPs had also the lowest 13 C elimination by breath and vise versa.…”

Section: Discussionsupporting

confidence: 70%

“…Thereafter, lipid extracts were hydrolyzed and the resulting fatty acid methylated (Lepage & Roy, 1986). The absolute fatty acid composition in plasma total lipids was analyzed using a gas chromatograph with a¯ame ionization detector (GCaFID, Perkin Elmer, Norwalk, Connecticut, USA) as described before (Vermunt et al, 2000).…”

Section: Blood Sampling and Analysismentioning

confidence: 99%

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The metabolism of linoleic acid in healthy subjects after intake of a single dose of 13C-linoleic acid

et al. 2001

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Objective: To investigate the in vivo oxidation of 13 C18X2n-6 and its conversion into longer-chain polyunsaturates (LCPs) in healthy subjects. Design: Blood samples were collected from six subjects before (fasted) and 7, 11 (non-fasted), 24, 48, 72, 168 and 336 h (fasted) after ingestion of a single bolus of 45 mg uniformly labeled 13 C18X2n-6 dissolved in 8 g olive oil. In three subjects, breath was also sampled and CO 2 production measured every hour during the ®rst 12 h. Subjects consumed their habitual diets. Plasma 13 C-enrichments were measured by GC-C-IRMS and fatty acid compositions by GCaFID. Setting: Maastricht University, Department of Human Biology. Subjects: Three men and three women, recruited by local advertisement. Results: The traceratracee ratio (TTR) of C18X2n-6 in plasma total lipids was already increased 5 h after tracer intake. The mean peak amount (AE s.e.m) of 13 C18X2n-6 (3.4AE 0.8 mg; 7.6% of dose) was found after about 17 h, 13 C18X3n-6 (0.018 AE 0.008 mg; 0.04% of dose) after 7 ± 48 h, and 13 C20X3n-6 (0.028 AE 0.011 mg; 0.06% of dose) after 48 ± 336 h. Time to peak TTRs of C20X4n-6 varied between subjects and were on average 0.022 AE 0.006 mg (0.05% of dose). The proportion of 13 C18X2n-6 recovered in breath after 12 h ranged between 16.8 and 25.1%. Conclusions: These ®ndings suggest that a single bolus of 45 mg U-13 C18X2n-6 can be used to study the oxidation of 13 C18X2n-6. However, because of the low TTRs for C20X4n-6, a higher dose is recommended for studying the conversion of 13 C18X2n-6 into LCPs. In addition, since only about 35% of the tracer was found in plasma total lipids and as 13 CO 2 in breath, it might be necessary to study other accessible lipid fractions as well to study the overall conversion of linoleic acid.

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Section: Discussionsupporting

confidence: 70%

Section: Blood Sampling and Analysismentioning

confidence: 99%

The metabolism of linoleic acid in healthy subjects after intake of a single dose of 13C-linoleic acid

et al. 2001

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“…No differences were observed on EPA and DHA levels in any of the piglet tissues between 2% and 1% maternal linseed oil feeding, indicating that the additional ALA was not further converted to its LC derivatives, but partially metabolized to 20:3n-3 and partially stored as ALA in the muscle tissue. Oxidation was not measured in this study, but it has already been suggested that diets high in ALA also increase the oxidation of ALA, thereby reducing its conversion to EPA (Vermunt et al, 2000).…”

mentioning

confidence: 77%

Effects of birth weight and maternal dietary fat source on the fatty acid profile of piglet tissue

Tanghe

Millet²,

Missotten

et al. 2014

Animal

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This study aimed to investigate the effects and possible interactions of birth weight and n-3 polyunsaturated fatty acid (PUFA) supplementation of the maternal diet on the fatty acid status of different tissues of newborn piglets. These effects are of interest as both parameters have been associated with pre-weaning mortality. Sows were fed a palm oil diet or a diet containing 1% linseed, echium or fish oil from day 73 of gestation. As fish oil becomes a scarce resource, linseed and echium oil were supplemented as sustainable alternatives, adding precursor fatty acids for DHA to the diet. At birth, the lightest and heaviest male piglet per litter were killed and samples from liver, brain and muscle were taken for fatty acid analysis. Piglets that died pre-weaning had lower birth weights than piglets surviving lactation (1.27 ± 0.04 v. 1.55 ± 0.02 kg; P < 0.001), but no effect of diet on mortality was found. Lower DHA concentrations were observed in the brain of the lighter piglets compared with their heavier littermates (9.46 ± 0.05 v. 9.63 ± 0.04 g DHA/100 g fatty acids; P = 0.008), suggesting that the higher incidence of pre-weaning mortality in low birth weight piglets may be related to their lower brain DHA status. Adding n-3 PUFA to the sow diet could not significantly reduce this difference in DHA status, although numerically the difference in the brain DHA concentration between the piglet weight groups was smaller when fish oil was included in the sow diet. Independent of birth weight, echium or linseed oil in the sow diet increased the DHA concentration of the piglet tissues to the same extent, but the concentrations were not as high as when fish oil was fed.

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“…Eicosapentaenoic (EPA; C20:5n-3) and docosahexaenoic acid (DHA; C22:6n-3) are n-3 HUFA and are primarily found in fatty fish. Although there is a biosynthetic pathway from the precursor -linolenic acid (C18:3n-3) into EPA and DHA (Emken et al 1994, Cho et al 1999, Salem et al 1999, Vermunt et al 2000, Pawlosky et al 2001, the quantitative contribution of this pathway to tissue EPA and DHA levels is unclear. In contrast to EPA and DHA, -linolenic acid is found in vegetables, walnuts and vegetable oils (e.g.…”

Section: Introductionmentioning

confidence: 99%

Raloxifene and hormone replacement therapy increase arachidonic acid and docosahexaenoic acid levels in postmenopausal women

Giltay¹,

Duschek²,

Katan³

et al. 2004

Journal of Endocrinology

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Estrogens may affect the essential n-6 and n-3 fatty acids arachidonic acid (AA; C20:4n-6) and docosahexaenoic acid (DHA; C22:6n-3). Therefore, we investigated the long-term effects of hormone replacement therapy and raloxifene, a selective estrogen-receptor modulator, in two randomized, double-blind, placebo-controlled studies. In study I, 95 healthy, non-hysterectomized, early postmenopausal women (age range 47-59 years) received one of the following treatments: daily raloxifene 60 mg (n=24), daily raloxifene 150 mg (n=23), 0·625 mg conjugated equine estrogens (CEE) plus 2·5 mg medroxyprogesterone acetate (MPA; n=24), or placebo (n=24). In study II, 30 men (age range 60-69 years) received daily 120 mg raloxifene (n=15) or placebo (n=15). In study I, plasma cholesteryl ester fatty acids were measured at baseline and after 6, 12, and 24 months in 83 (drop out rate 13%), 73 (23%), and 70 (25%) women respectively. In study II, fatty acids were measured at baseline and after 3 months in 29 men (drop out rate 3%). In postmenopausal women, administration of 150 mg raloxifene increased AA by a mean of +6·1% (P=0·055, not significant). Administration of CEE plus MPA increased AA by +14·1% (P<0·0005). Mean changes in DHA were +22·1% (P=0·003) and +14·9% (P=0·047) respectively, as compared with placebo. In men, 120 mg raloxifene for 3 months did not significantly affect AA (-5·2%; P=0·342) or DHA (+4·0%; P=0·755), but it increased testosterone levels by +19·8% (P=0·006). Administration of raloxifene 150 mg/day as well as CEE plus MPA to postmenopausal women increases the proportion of AA and DHA in plasma cholesteryl esters during a follow-up of 2 years. Short term administration of raloxifene in elderly men did not affect AA or DHA. The synthesis of AA and DHA from precursors may be enhanced through an estrogen receptor-dependent pathway.

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Effects of dietary α‐linolenic acid on the conversion and oxidation of¹³C‐α‐linolenic acid

Cited by 126 publications

References 24 publications

The metabolism of linoleic acid in healthy subjects after intake of a single dose of 13C-linoleic acid

The metabolism of linoleic acid in healthy subjects after intake of a single dose of 13C-linoleic acid

Effects of birth weight and maternal dietary fat source on the fatty acid profile of piglet tissue

Raloxifene and hormone replacement therapy increase arachidonic acid and docosahexaenoic acid levels in postmenopausal women

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Effects of dietary α‐linolenic acid on the conversion and oxidation of13C‐α‐linolenic acid

Cited by 126 publications

References 24 publications

The metabolism of linoleic acid in healthy subjects after intake of a single dose of 13C-linoleic acid

The metabolism of linoleic acid in healthy subjects after intake of a single dose of 13C-linoleic acid

Effects of birth weight and maternal dietary fat source on the fatty acid profile of piglet tissue

Raloxifene and hormone replacement therapy increase arachidonic acid and docosahexaenoic acid levels in postmenopausal women

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Effects of dietary α‐linolenic acid on the conversion and oxidation of¹³C‐α‐linolenic acid