E-Poster Presentation ESA-SRB-ANZBMS 2021

Nutrient-sensing components of the mouse intestine during pregnancy (#554)

Georgia S Clarke 1 2 3 , Sharon R Ladyman 4 , Richard L Young 1 3 , Kathryn L Gatford 2 3 , Amanda J Page 1 3
  1. Nutrition, Diabetes & Gut Health, 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: Increased maternal food intake during pregnancy is essential for normal fetal growth, while under- or over-nutrition increases pregnancy complications and adult disease risks in progeny. Meal termination occurs, at least in part, through nutrient induced release of satiety hormones from intestinal enteroendocrine cells (EECs). This occurs upon activation of specific EEC nutrient-sensors by luminal carbohydrates, fatty acids and proteins. It is unknown whether intestinal nutrient-sensing adapts to facilitate increased food intake during pregnancy.

Aims: To measure food intake and intestinal expression of nutrient-sensors and satiety hormones across pregnancy in mice.

Methods: Female C57BL/6J mice (10-12wk) were mated and randomised to early- (6.5d), mid- (12.5d) or late-stage pregnancy (17.5d) groups, or age matched, non-pregnant controls (N=10-12/stage). Mice were housed in Promethion cages for the duration of pregnancy to monitor body weight and food intake behaviour. Quantitative RT-PCR was used to determine the relative expression of intestinal fatty acid, protein and carbohydrate sensors and hormones in the duodenum, jejunum and ileum across pregnancy groups (N=6-8/stage).

Results: Pregnant mice were heavier from day 7 and ate more by mid-pregnancy, predominantly due to an increase in meal size in the light phase (P<0.05). The duodenal expression of transcripts for free fatty acid receptor 4 (FFAR4) and the protein receptor, GPR93, was lower (P<0.05) and for FFAR2 was higher (P<0.05) as pregnancy progressed. Transcript levels for cholecystokinin and pro-glucagon were unchanged in the duodenum across pregnancy. 

Conclusion: Maternal food intake increases during pregnancy in support of fetal development.  Region-specific reductions in intestinal FFAR4 and GPR93, if present as proteins, may reduce fatty acid and protein sensing and the subsequent deployment of satiety hormones, to promote food intake during pregnancy.  Understanding the plasticity of nutrient-sensing in pregnancy has the potential to yield new strategies that optimise maternal nutrition and safeguard the lifespan health of progeny.