Evidence map›Paper›PMID 34230622›Full record

ArticlePediatric research2022

Sex-specific alterations in hepatic cholesterol metabolism in low birth weight adult guinea pigs.

Ousseynou Sarr, Katherine E Mathers, Christina Vanderboor, Kristina Wiggers, Aditya Devgan, Daniel B Hardy, Lin Zhao, Timothy R H Regnault

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Article in Pediatric research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. PlacentaAmerican journal of physiology. Endocrinology and metabolism · 2025
    Article
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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

8 authors at 1 institution in 1 country.

Ousseynou SarrDepartment of Physiology and Pharmacology, Western University, London, ON, Canada.
Katherine E MathersDepartment of Physiology and Pharmacology, Western University, London, ON, Canada.
Christina VanderboorDepartment of Physiology and Pharmacology, Western University, London, ON, Canada.
Kristina WiggersDepartment of Physiology and Pharmacology, Western University, London, ON, Canada.
Aditya DevganDepartment of Physiology and Pharmacology, Western University, London, ON, Canada.
Daniel B HardyDepartment of Physiology and Pharmacology, Western University, London, ON, Canada.
Lin ZhaoDepartment of Physiology and Pharmacology, Western University, London, ON, Canada.
Timothy R H RegnaultDepartment of Physiology and Pharmacology, Western University, London, ON, Canada. tim.regnault@uwo.ca.
Western University · CA

Funding

CIHR MOP-209113
6 · The paper itself

Abstract

backgroundIntrauterine growth restriction and low birth weight (LBW) have been widely reported as an independent risk factor for adult hypercholesterolaemia and increased hepatic cholesterol in a sex-specific manner. However, the specific impact of uteroplacental insufficiency (UPI), a leading cause of LBW in developed world, on hepatic cholesterol metabolism in later life, is ill defined and is clinically relevant in understanding later life liver metabolic health trajectories.

methodsHepatic cholesterol, transcriptome, cholesterol homoeostasis regulatory proteins, and antioxidant markers were studied in UPI-induced LBW and normal birth weight (NBW) male and female guinea pigs at 150 days.

resultsHepatic free and total cholesterol were increased in LBW versus NBW males. Transcriptome analysis of LBW versus NBW livers revealed that "cholesterol metabolism" was an enriched pathway in LBW males but not in females. Microsomal triglyceride transfer protein and cytochrome P450 7A1 protein, involved in hepatic cholesterol efflux and catabolism, respectively, and catalase activity were decreased in LBW male livers. Superoxide dismutase activity was reduced in LBW males but increased in LBW females.

conclusionsUPI environment is associated with a later life programed hepatic cholesterol accumulation via impaired cholesterol elimination in a sex-specific manner. These programmed alterations could underlie later life cholesterol-induced hepatic lipotoxicity in LBW male offspring. IMPACT: Low birth weight (LBW) is a risk factor for increased hepatic cholesterol. Uteroplacental insufficiency (UPI) resulting in LBW increased hepatic cholesterol content, altered hepatic expression of cholesterol metabolism-related genes in young adult guinea pigs. UPI-induced LBW was also associated with markers of a compromised hepatic cholesterol elimination process and failing antioxidant system in young adult guinea pigs. These changes, at the current age studied, were sex-specific, only being observed in LBW males and not in LBW females. These programmed alterations could lead to further hepatic damage and greater predisposition to liver diseases in UPI-induced LBW male offspring as they age.

Indexed as

AntioxidantsLiver DiseasesAnimalsBirth WeightCholesterolCytochrome P-450 Enzyme SystemFemaleGuinea PigsHumansInfant, Low Birth WeightInfant, NewbornMaleAntioxidantsCholesterolCytochrome P-450 Enzyme System

Identifiers

PMID34230622
OpenAlexW3180998902

What OpenQuestion holds

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Registered trials

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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.