Effect of dietary polyunsaturated fatty acids on uterine prostaglandin synthesis in the cow.
Dietary polyunsaturated fatty acid (PUFA) intake in humans can affect the incidence of a variety of diseases including coronary heart disease. Feeding high PUFA diets to cows can alter the PUFA content of milk for human consumption. PUFAs supply the precursors for prostaglandin (PG) synthesis and PGs in turn influence many aspects of reproduction. This study examined the effects of a control (CONT), a high n-6 PUFA diet (derived from protected soya) and a high n-3 diet (derived from protected linseed) on uterine PG synthesis in the lactating dairy cow. Endometrial explants obtained on days 15-17 of the oestrous cycle were cultured for an initial 42 h in vitro in fully defined medium (basal production) and then challenged with control medium, oxytocin (OT; 20 or 200 nM) or calcium ionophore A23187 (CaI; 10 microM). PGF(2 alpha), PGE(2) and 6-keto-PGF(1 alpha) were measured in the spent medium. The experiments were repeated using tissue from two groups of cows, nine in Experiment 1 (three cows per diet) and seven in Experiment 2 (four CONT and three n-6). Results of the two experiments were consistent. The basal concentrations of all three PGs were significantly lower (>50% reduction) in the n-6-fed group in comparison with CONT and n-3 groups. The n-3 diet did not alter basal PGF(2 alpha) and PGE(2) but increased 6-keto-PGF(1 alpha). The n-6 diet also inhibited the ability of the tissue to respond to both OT and CaI, with significant reductions in the stimulated levels of all three PGs. In contrast, the n-3 diet only had minor effects; it did not alter the response to OT but did reduce the long-term response to CaI at 24 h post treatment. In conclusion, dietary PUFA intake can inhibit PG production in bovine endometrial explants, with a more pronounced effect following n-6 rather than n-3 supplementation. These data suggest that a high n-6 diet reduces the endometrial capacity to produce PGs and may therefore have implications for the control of luteolysis and other PG-mediated events such as ovulation.
Cheng
Z
Z
Reproduction and Development Group, Department of Veterinary Basic Sciences, Royal Veterinary College, Boltons Park, Hawkshead Road, Potters Bar, Hertfordshire EN6 1NB, UK.
Robinson
R S
RS
Pushpakumara
P G
PG
Mansbridge
R J
RJ
Wathes
D C
DC
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002417:Cattle / Q000378:metabolism*; D046508:Culture Techniques; D004032:Diet; D004042:Dietary Fats, Unsaturated / Q000494:pharmacology*; D015237:Dinoprost / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D004717:Endometrium / Q000187:drug effects* / Q000378:metabolism; D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology*; D005260:Female; D010121:Oxytocin / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis*; D014280:Triglycerides / Q000494:pharmacology
D004042:Dietary Fats, Unsaturated; D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6; D005231:Fatty Acids, Unsaturated; D011453:Prostaglandins; D014280:Triglycerides; C077446:Pikasol; D000001:Calcimycin; D010121:Oxytocin; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D015232:Dinoprostone