The effect of a diet supplemented with the n-6 polyunsaturated fatty acid linoleic acid on prostaglandin production in early- and late-pregnant ewes

Abstract

Polyunsaturated fatty acids derived from the diet are incorporated into cell membranes where they act as precursors for prostaglandin (PG) synthesis. Linoleic acid (LA; 18:2 n-6) is a major constituent of plant oils and its consumption in Westernized populations is increasing. This study investigated the influence of LA on PG production by the uterus and placenta. Pregnant ewes were fed a control or an LA-enriched diet. Oxytocin (OT) was injected on day 45 (early) or day 133 (late) of gestation to measure the release of 13,14-dihydro-15-keto PGF 2 (PGFM). Ewes were killed on day 46 or day 138 for collection of uterine intercaruncular endometrium and fetal allantochorion. Basal and stimulated PG release from explant cultures was assessed before and after in vitro treatment with OT, lipopolysaccharide (LPS), dexamethasone (DEX) or calcium ionophore (CaI). Expression of cyclooxygenase (COX)-1 and COX-2 was determined by Western blot in endometrium of late-gestation ewes. Circulating PGFM levels in vivo did not differ according to diet but there were highly significant differences in the release of PGs in vitro. Basal production of PGF 2 and PGE 2 by the endometrium and of PGE 2 by the allantochorion were all higher in tissues from LA-supplemented ewes. Endometrial tissues produced more PG following OT and CaI treatment, whereas DEX inhibited production of both PGs at both stages of gestation. In allantochorion collected at day 46 LPS did not significantly alter PGE 2 release and DEX increased output, whereas at day 138 LPS was stimulatory but DEX was inhibitory. These data show that a high-LA diet can significantly increase the ability of both endometrium and placental tissues to produce PGs in vitro. This effect of diet may only become apparent after a sustained period of PG release, so was not seen following the brief pulse caused by OT treatment in vivo. As COX protein levels were unaltered, the main influence was likely to be via conversion of LA to arachidonic acid, providing an increased supply of precursor. These results support previous studies which suggest that alterations in dietary polyunsaturated fatty acids may influence the time of labour.

Expression of acyl‐CoA synthetase 5 in human endometrium and in endometrioid adenocarcinomas

“…There is general agreement that fatty acid metabolism is important for homeostasis in the endometrium as well as for the physiological interaction of the endometrial–ovarian axis 13 . Endometrial expression and the function of several enzymes involved in fatty acid metabolism such as ACSs have been investigated in the past, 2,13 but there is no detailed study about the expression of the isoform ACS5 in human endometrium under normal or pathological conditions. The first evidence for the expression of the ACS isoform ACS5 in the human uterus came from Northern blot hybridization reported by Yamashita 8 .…”

The potential for improving physiological, behavioural and immunological responses in the neonatal lamb by trace element and vitamin supplementation of the ewe

“…Administration of n-3-enhanced (EPA/DHA) intralipid delayed parturition in sheep (Baguma-Nibasheka et al, 1999). In addition, a series of studies (Cheng et al, 2003(Cheng et al, , 2005a(Cheng et al, and 2005bElmes et al, 2004 and have demonstrated the opposite effect. In vitro and in vivo, increasing n-6 fatty acid supply increased 2-series prostaglandin production by late-pregnancy ovine endometrium.…”

The Effects of Maternal Dietary Docosahexaenoic Acid Intake on Rat Pup Myelin and the Auditory Startle Response

“…However, pregnant and lactating women who consume greater quantities of DHA have lower levels of AA in their milk and blood, and AA levels are lower in their offspring [17,20,55,58,59] . While the inclusion of AA in postnatal diets offsets the negative effects of high n3 diets, supplementation of pregnant women with AA or its precursor is not recommended since this may increase placental production of prostaglandins that can increase the risk of preterm labor [55,[60][61][62] .…”