Evidence map›Paper›PMID 34299119›Full record

ArticleInternational journal of molecular sciences2021

In Utero Exposure to Δ9-Tetrahydrocannabinol Leads to Postnatal Catch-Up Growth and Dysmetabolism in the Adult Rat Liver.

Shelby L Oke, Kendrick Lee, Rosemary Papp, Steven R Laviolette, Daniel B Hardy

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Prenatal Cannabis and Tobacco: Studies in Animal Models.Advances in experimental medicine and biology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Early Life Nutrition and the Development of Offspring Metabolic Health.International journal of molecular sciences · 2022
    Article
  13. Article
  14. Metabolic Consequences of Gestational Cannabinoid Exposure.International journal of molecular sciences · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Shelby L OkeDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, 1151 Richmond Street, London, ON N6A 5C1, Canada.
Kendrick LeeDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, 1151 Richmond Street, London, ON N6A 5C1, Canada.
Rosemary PappDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, 1151 Richmond Street, London, ON N6A 5C1, Canada.
Steven R LavioletteDepartment of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, 1151 Richmond Street, London, ON N6A 5C1, Canada.
Daniel B HardyDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, 1151 Richmond Street, London, ON N6A 5C1, Canada.ORCID 0000-0001-5445-273X
Western University · CA

Funding

Canadian Heart and Stroke Foundation G-19-0026343CIHR CRU1126Natural Sciences and Engineering Research Council CGS-D
6 · The paper itself

Abstract

The rates of gestational cannabis use have increased despite limited evidence for its safety in fetal life. Recent animal studies demonstrate that prenatal exposure to Δ9-tetrahydrocannabinol (Δ9-THC, the psychoactive component of cannabis) promotes intrauterine growth restriction (IUGR), culminating in postnatal metabolic deficits. Given IUGR is associated with impaired hepatic function, we hypothesized that Δ9-THC offspring would exhibit hepatic dyslipidemia. Pregnant Wistar rat dams received daily injections of vehicular control or 3 mg/kg Δ9-THC i.p. from embryonic day (E) 6.5 through E22. Exposure to Δ9-THC decreased the liver to body weight ratio at birth, followed by catch-up growth by three weeks of age. At six months, Δ9-THC-exposed male offspring exhibited increased visceral adiposity and higher hepatic triglycerides. This was instigated by augmented expression of enzymes involved in triglyceride synthesis (ACCα, SCD, FABP1, and DGAT2) at three weeks. Furthermore, the expression of hepatic DGAT1/DGAT2 was sustained at six months, concomitant with mitochondrial dysfunction (i.e., elevated p66shc) and oxidative stress. Interestingly, decreases in miR-203a-3p and miR-29a/b/c, both implicated in dyslipidemia, were also observed in these Δ9-THC-exposed offspring. Collectively, these findings indicate that prenatal Δ9-THC exposure results in long-term dyslipidemia associated with enhanced hepatic lipogenesis. This is attributed by mitochondrial dysfunction and epigenetic mechanisms.

Indexed as

LipogenesisAnimalsAnimals, NewbornDronabinolDyslipidemiasFemaleHallucinogensLiverMalePregnancyPrenatal Exposure Delayed EffectsRatsRats, WistarDronabinolHallucinogensintrauterine growth restrictionlivermetabolismmiR-203a-3pmiR-29a/b/cmitochondriaoxidative stresstriglyceridesΔ9-tetrahydrocannabinol

Identifiers

PMID34299119
PMCPMC8305322
OpenAlexW3181893485

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.