Oral 63rd Endocrine Society of Australia Annual Scientific Meeting 2020

Plasticity of gastric satiety signals during pregnancy and in response to pregnancy hormones. (#30)

Georgia S Clarke 1 2 3 , Hui Li 1 3 , Stewart Christie 1 3 , Sharon R Ladyman 4 , Stephen J Kentish 1 3 , Richard L Young 1 3 , Kathryn L Gatford 1 2 3 , Amanda J Page 1 3
  1. Lifelong Health Theme, South Australian Health and Medical Research Institue, Adelaide, South Australia, Australia
  2. Robinson Research Institute, University of Adelaide, adelaide, South Australia, Australia
  3. University of Adelaide, Adelaide, SOUTH AUSTRALIA, Australia
  4. Centre for Neuroendocrinlogy and Department of Anatomy, University of Otago, Dunedin, New Zealand

Background: Gastric vagal afferents (GVAs) sense food related mechanical stimuli and signal to the central nervous system, to integrate control of meal termination. Maternal food intake increases during pregnancy to ensure normal fetal growth and to maximise progeny survival and health.

Aims: This study evaluated changes in GVA function during pregnancy and in response to pregnancy-related hormones

Methods: Female C57BL/6J mice (10-12wk) were mated and randomised to non-pregnant, early (6.5 day (d), N=10), mid (12.5d, N=10) or late-pregnancy (17.5d, N=11) groups. Mice were individually housed in Promethion metabolic cages throughout pregnancy, then the mechanosensitivity of GVAs was determined using an in vitro tissue preparation. Effects of the pregnancy hormones oestradiol (10-1000pM), progesterone (30-300nM), prolactin (30-300ng/ml), and growth hormone (3-300ng/ml) on GVA mechanosensitivity were determined separately in 8-week-old female C57BL/6 non-pregnant mice.

Results: Pregnant mice were heavier from d7 (P<0.05) and ate more by mid-pregnancy, predominantly due to increased meal size (P<0.05). The mechanosensitivity of GVAs to stretch (0.5-5g) decreased as pregnancy progressed (P<0.001), and correlated negatively with meal size (P=0.032). Oestradiol increased (P < 0.05), growth hormone decreased (P< 0.05) and prolactin and progesterone had no effect on GVA responses to stretch (3g) in non-pregnant mice.

Conclusions: The mechanosensitivity of GVAs is attenuated during pregnancy and associated with increased food intake. These GVA adaptations are likely to support increases in food intake to meet the energy demands of the growing fetus, and may be driven by increases in circulating levels of growth hormone during pregnancy.