Oral Presentation ESA-SRB-NZSE-CaSR 2026 in conjunction with ENSA

Cannabis and the potential drivers for fat accumulation in the human placenta (144073)

Michael Patterson 1 , Min-Tz Weng 2 , Kathryn Steadman 2 , Elizabeth Burmeister 3 , Angela Ratsch 1 2 3 , Georgia Kafer 1
  1. School of Health, University of the Sunshine Coast, Moreton Bay, QLD, Australia
  2. University of Queensland, Brisbane, QLD, Australia
  3. Research Services, Wide Bay Hospital and Health Service, Hervey Bay, QLD, Australia

1. Background

Cannabis use during pregnancy is increasing, yet its effects on the placenta are poorly understood. Tetrahydrocannabinol (THC) and cannabidiol (CBD) are phytocannabinoids that interact with peroxisome proliferator-activated receptor gamma (PPARy), a nuclear receptor that regulates adipogenic differentiation of mesenchymal stem cells, present in the placenta. A scoping review (Patterson et al., under consideration) identified that placental lipid accumulation is poorly characterised with unknown health consequences. Interestingly, we have observed increased placental lipid accumulation in cannabis-exposed pregnancies (1). We therefore investigated how cannabis exposure alters placental form and function in third-trimester human placental tissue. 

2. Methods

At delivery, placental villous tissue was collected from four separate regions, washed in PBS and stored in RNAlater (n=59) (1). Total lipids were extracted using an adapted Folch method (2), quantified (colourimetric triglyceride kit) and profiled by GC/MS (n=57). Total RNA was extracted, DNAse treated (TurboDNAse) and sequenced (Nanopore, NGS, n=59). Isolated RNA was also reverse transcribed, and qRT-PCR was performed for genes of interest (SYBR technology, normalised to GAPDH, n=19). All analyses were performed in relation to known exposures of THC, CBD, nicotine and anabasine, quantified using LC-MS/MS in maternal urine samples collected at time of delivery. Groups were compared by one-way ANOVA with Tukey post-hoc or Kruskal-Wallis for non-normally distributed measures. 

3. Results

THC exposure (n=4) was associated with significantly increased placental triglycerides versus nicotine-exposed (n=9, p=0.0244) and non-exposed (n=17, p=0.0265) groups (Tukey post-hoc). Separately, THC exposure (n=4) caused significantly increased PPARy expression in placental villi versus nicotine alone (n=4, p=0.0361, Kruskal-Wallis post-hoc). RNAseq analysis further indicates that THC, CBD and nicotine exposure variations are associated with altered, diverse placental gene expression profiles. 

4. Conclusion

These findings suggest gestational cannabis exposure may be associated with increased placental lipid accumulation and transcriptional changes, warranting further investigation. 

  1. Ratsch A, Burmeister EA, Bird AV, Bonner AJ, Miller UG, Speedy AM, Douglas G, Ober S, Woolcock Nee Geary-Laverty A, Blair Nee Murdoch S, Weng MT, Miles JA, Steadman KJ. Tobacco, nicotine, and cannabis use and exposure in an Australian Indigenous population during pregnancy: A protocol to measure parental and foetal exposure and outcomes. PLoS One. 2024 Sep 6;19(9):e0300406. doi: 10.1371/journal.pone.0300406. PMID: 39240849; PMCID: PMC11379133.
  2. Folch J, Lees M, Sloane Stanley GH. A simple method for the isolation and purification of total lipides from animal tissues. J Biol Chem. 1957 May;226(1):497-509. PMID: 13428781.