Poster Presentation ESA-SRB-APEG-NZSE 2022

Plasticity in gastric satiety signals during pregnancy and the impact of diet-induced obesity   (#392)

Georgia S Clarke 1 2 3 , Hui Li 1 3 , Jessica P Ward 1 2 3 , Lisa M Nicholas 2 , Sharon R Ladyman 4 , Kathryn L Gatford 1 2 , 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. Vagal Afferent Research Group, University of Adelaide, Adelaide, South Australia, Australia
  4. Centre for Neuroendocrinlogy and Department of Anatomy, University of Otago, Dunedin, New Zealand

Maternal obesity increases the risk of poor pregnancy outcomes and adulthood disease in the offspring. Gastric vagal afferents (GVAs) sense food-related mechanical stimuli and signal to the central nervous system to integrate control of meal termination. Both pregnancy and diet-induced obesity are independently associated with dampened mechanosensitivity of GVAs and increased food intake. Whether an obesogenic diet impacts pregnancy-related adaptations in GVA satiety is unknown. Therefore, we aimed to determine how food intake and GVA function change in response to pregnancy in a mouse model of diet-induced obesity.

Three-week-old female Glu Venus-expressing mice were fed a standard laboratory diet (SLD) or high-fat, high-sugar diet (HFHSD) for 12 weeks, then half of each group were mated to generate late pregnant (d17.5; SLD N=7, HFHSD N=9) or non-pregnant (SLD N=8, HFHSD N= 10) groups. Individual body weight and food intake was automatically monitored for a week prior to humane killing and tissue collection at 0700h for the in vitro single fibre GVA recording preparation.

Diet did not affect weight of SLD and HFHSD mice during pregnancy (P=0.541). On the final day of study (d16.5-17.5), food intake and meal size in the light phase were higher in pregnant than non-pregnant mice (each P<0.001). Food intake (P=0.026), meal size (P<0.001) and meal duration (P=0.029) were each lower in HFHS than SLD mice during the same period. In SLD mice, the response of tension sensitive GVAs to stretch tended to be lower in pregnancy (P=0.051), but this response did not differ between HFHSD pregnant and non-pregnant mice.

In conclusion, reduced mechanosensitivity of GVAs during pregnancy would partly permit increased food intake during pregnancy. Our data so far suggests that a HFHSD appears to prevent adaptation of the GVA signalling during pregnancy.