Organ weight at birth can have an important influence of postnatal morbidity and mortality. One factor that can influence size at birth is maternal parity for which birth weight may be expected to increase, even when maternal body weight has changed very little between first and second pregnancies. The extent to which maternal parity can have a differential effect on adipose tissue deposition and its leptin synthetic capacity is not known.

Ten twin bearing sheep of similar body weight were entered into the study of which 5 were primiparous (P) and 5 multiparous (M). All ewes were fed 100 % of total metabolisable energy (ME) requirements throughout gestation and all ewes delivered normally at term. An intravenous overdose of sodium pentabarbitone was used to humanely euthanase one lamb at one day of age and the other at one month of age (n = 5 per group). Tissue sampling was performed and samples immediately snap frozen in liquid nitrogen and stored at -80 °C until analysis. Total RNA was extracted and RT-PCR analysis was performed using oligonucleotide primers specific to ovine leptin (forward 5′-CAC CAA AAC CCT CAT CAA GAC G-3′ and reverse 5′-ACA TTT CTG GAA GGC AGA CTGG-3′, amplicon size 192bp) (Bispham et al. 2003). Results are expressed in arbitrary units (a.u.; mean plus/minus s.e.m) as a ratio of an 18S rRNA internal control. Statistical differences were analysed using Kruskal-Wallis and Mann-Whitney U tests.

At one day of postnatal age lambs born to multiparous ewes had significantly lower expression levels of leptin than there primiparous counterparts (P: 88.9 ± 11.3; M: 47.7 ± 10.1 a.u. (P < 0.05)). This difference between groups persisted up to one month of age (P: 75.3 ± 17.5; M: 30.5 ± 7.3 a.u. (P < 0.05)) when the offspring of the primiparous mothers possessed more fat (P 153 ± 10: M 108 ± 14 g (P < 0.01). There was no difference in body weights between groups at either 1 or 30 days of age.

Maternal parity is a major factor determining fat deposition and leptin synthetic capacity over the first month of postnatal life. The extent to which the enhanced fat mass and greater potential leptin production may contribute to altered fat deposition in later life remains to be established.