Abstract

Maternal obesity is associated with prolonged and dysfunctional labour, potentially through decreased synthesis of prostaglandins that stimulate myometrial contractions. We assessed the impact of maternal obesity on concentrations of precursor fatty acids (FA) for prostaglandin synthesis and whether any changes could be reversed by improved nutrition post-conception. Wistar rats were fed control (CON) or High-Fat, High-cholesterol (HFHC) diets 6 weeks before mating. At conception half the dams switched diets providing 4 dietary groups: (1) CON, (2) HFHC, (3) CON-HFHC or (4) HFHC-CON. During parturition rats were euthanized and FA composition of plasma, liver and uterus determined. Visceral fat was doubled in rats exposed to the HFHC diet prior to and/or during pregnancy compared to CON. HFHC diet increased MUFAs but decreased omega-3 and omega-6 PUFAs in plasma and liver. Uterine omega-3 FA concentrations were halved in HFHC versus CON rats, but all other FAs were similar. Switching from HFHC to CON diet at conception restored all FA profiles to those seen in CON rats. The increased MUFA and decreased PUFA concentrations in obese HFHC dams may contribute to aberrant prostaglandin synthesis and dysfunctional myometrial activity and it may be possible to reverse these changes, and potentially improve labour outcomes, by improving nutrition at conception.

Highlights

  • Maternal obesity is associated with prolonged and dysfunctional labour, potentially through decreased synthesis of prostaglandins that stimulate myometrial contractions

  • Dietary alteration of prostaglandin synthesis has been proposed to occur through n-3 and n-6 polyunsaturated fatty acids (PUFAs), such as DGLA (20:3, n-6) and EPA competing with AA for incorporation into phospholipids of the plasma membrane[21,22] and processing by desaturase[23,24] and COX-2 enzymes that synthesise long chain PUFAs and prostaglandins respectively

  • Visceral fat mass was 2-fold higher in rats exposed to the HFHC diet either before and/or post-conception compared to the CON group (Fig. 2)

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Summary

Introduction

Maternal obesity is associated with prolonged and dysfunctional labour, potentially through decreased synthesis of prostaglandins that stimulate myometrial contractions. The increased MUFA and decreased PUFA concentrations in obese HFHC dams may contribute to aberrant prostaglandin synthesis and dysfunctional myometrial activity and it may be possible to reverse these changes, and potentially improve labour outcomes, by improving nutrition at conception. The fact that the omega-3 and omega-6 fats give rise to PGs with distinct biological activities has led to suggestions that the dietary balance of omega-6 and omega-3 fatty acids may play a key regulatory role in labour and parturition, the physiological processes requiring prostaglandin synthesis This is supported by human and animal studies that have shown a significant increase in the risk of premature labour when humans or animal consume diets rich in n-6 PUFA13,14. Dietary alteration of prostaglandin synthesis has been proposed to occur through n-3 and n-6 PUFAs, such as DGLA (20:3, n-6) and EPA competing with AA for incorporation into phospholipids of the plasma membrane[21,22] and processing by desaturase[23,24] and COX-2 enzymes that synthesise long chain PUFAs and prostaglandins respectively

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