ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2006) 12 P101

The effects of feeding an n-3 polyunsaturated fatty acid (PUFA) rich diet on ovarian function in the Welsh mountain ewe

JM Naddafy, EC Chin, Z Cheng, JS Brickell, DC Wathes & DRE Abayasekara

Royal Veterinary College, London, United Kingdom.

Polyunsaturated fatty acids (PUFA) act as precursors for prostaglandin (PG) synthesis. PGs both inhibit and stimulate ovarian steroidogenesis. We have therefore examined the hypothesis that high n-3 PUFA diets affect ovarian steroid synthesis through modulating prostaglandin synthesis.

Welsh mountain ewes were individually fed a control diet or a diet containing linseed (high in n-3 PUFA) for 6 weeks. To assess the impact of the diet during different stages of the oestrous cycle, ewes were slaughtered during either the early (days 4–5: n=8) or late luteal phase (day 14: n=9) of the cycle. Blood samples were collected for the analysis of plasma progesterone (P4), and 13,14-dihydro-15 keto prostaglandin F (PGFM: the stable metabolite of prostaglandin F) by specific immunoassays. Ovarian and uterine tissue lysates were analysed by western blotting for expression of key regulators of PG (cyclooxygenase-2: COX-2) and steroid hormones (steroidogenic acute regulatory protein: StAR) synthesis.

The high n-3 PUFA diet significantly decreased the number of PGFM peaks between days 13–16 (control ewes: n=6, 6.2±0.48; n-3 ewes: n=8, 3.9±0.74, P<0.05) and increased the levels of P4 (ng/ml) on days 14.5–16 (control ewes: n=6, 0.32±0.12; n-3 ewes: n=5, 0.71±0.15, P<0.05) of the oestrous cycle. Moreover, on days 4–5 of the oestrous cycle, levels of expression of StAR and COX-2 were significantly lower in ovaries as was uterine expression of COX-2 on day 14 from n-3 PUFA fed animals. We therefore conclude that a high n-3 PUFA diet extends the luteal phase of the oestrous cycle by inhibiting uterine release of PGF (through inhibiting uterine COX-2 expression). The effects of the PUFA diet on StAR expression may be either direct or indirect due to lack of luteotrophic support from prostaglandin E2 as a consequence of decreased ovarian COX-2 expression.

Supported by the Wellcome Trust and BBSRC.

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