Evidence map›Paper›PMID 34663892›Full record

ArticleInternational journal of obesity (2005)2022

Effects of maternal diet-induced obesity on metabolic disorders and age-associated miRNA expression in the liver of male mouse offspring.

Laís Vales Mennitti, Asha A M Carpenter, Elena Loche, Lucas C Pantaleão, Denise S Fernandez-Twinn, Josca M Schoonejans, Heather L Blackmore, Thomas J Ashmore, Luciana Pellegrini Pisani, John A Tadross and 2 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of obesity (2005), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

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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

12 authors at 2 institutions in 2 countries.

Laís Vales Mennitti *Department of Bioscience, Laboratory of Nutrition and Endocrine Physiology, Federal University of São Paulo, Santos, 11015-020, Brazil.
Asha A M Carpenter *Metabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom.
Elena LocheMetabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom.
Lucas C PantaleãoMetabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom.
Denise S Fernandez-TwinnMetabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom.ORCID http://orcid.org/0000-0003-2610-277X
Josca M SchoonejansMetabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom.ORCID http://orcid.org/0000-0003-2893-7199
Heather L BlackmoreMetabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom.
Thomas J AshmoreMetabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom.
Luciana Pellegrini PisaniDepartment of Bioscience, Laboratory of Nutrition and Endocrine Physiology, Federal University of São Paulo, Santos, 11015-020, Brazil.
John A TadrossMetabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom.ORCID http://orcid.org/0000-0002-8424-1252
Iain HargreavesDepartment of Pharmacy and Biomolecular Science, Liverpool John Moores University, Byrom Street, Liverpool, L3 5UA, United Kingdom.
Susan E OzanneMetabolic Research Laboratories and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 OQQ, United Kingdom. seo10@cam.ac.uk.ORCID http://orcid.org/0000-0001-8753-5144
University of Cambridge · GBLiverpool John Moores University · GB

Funding

British Heart Foundation FS/16/53/32729British Heart Foundation RG/17/12/33167Department of Health CL-2019-14-504Medical Research Council MC_UU_00014/4Medical Research Council MC_UU_00014/5Medical Research Council MC_UU_12012/4
6 · The paper itself

Abstract

objectiveThis study investigated the effect of maternal obesity on aged-male offspring liver phenotype and hepatic expression of a programmed miRNA.

methodsA mouse model (C57BL/6 J) of maternal diet-induced obesity was used to investigate fasting-serum metabolites, hepatic lipid content, steatosis, and relative mRNA levels (RT-PCR) and protein expression (Western blotting) of key components involved in hepatic and mitochondrial metabolism in 12-month-old offspring. We also measured hepatic lipid peroxidation, mitochondrial content, fibrosis stage, and apoptosis in the offspring. To investigate potential mechanisms leading to the observed phenotype, we also measured the expression of miR-582 (a miRNA previously implicated in liver cirrhosis) in 8-week-old and 12-month-old offspring.

resultsBody weight and composition was similar between 8-week-old offspring, however, 12-month-old offspring from obese mothers had increased body weight and fat mass (19.5 ± 0.8 g versus 10.4 ± 0.9 g, p < 0.001), as well as elevated serum levels of LDL and leptin and hepatic lipid content (21.4 ± 2.1 g versus 12.9 ± 1.8 g, p < 0.01). This was accompanied by steatosis, increased Bax/Bcl-2 ratio, and overexpression of p-SAPK/JNK, Tgfβ1, Map3k14, and Col1a1 in the liver. Decreased levels of Bcl-2, p-AMPKα, total AMPKα and mitochondrial complexes were also observed. Maternal obesity was associated with increased hepatic miR-582-3p (p < 0.001) and miR-582-5p (p < 0.05). Age was also associated with an increase in both miR-582-3p and miR-582-5p, however, this was more pronounced in the offspring of obese dams, such that differences were greater in 12-month-old animals (-3p: 7.34 ± 1.35 versus 1.39 ± 0.50, p < 0.0001 and -5p: 4.66 ± 1.16 versus 1.63 ± 0.65, p < 0.05).

conclusionOur findings demonstrate that maternal diet-induced obesity has detrimental effects on offspring body composition as well as hepatic phenotype that may be indicative of accelerated-ageing phenotype. These whole-body and cellular phenotypes were associated with age-dependent changes in expression of miRNA-582 that might contribute mechanistically to the development of metabolic disorders in the older progeny.

Indexed as

Age FactorsAnimalsDisease Models, AnimalFeeding BehaviorFemaleGene ExpressionLiverMaternal ExposureMetabolic DiseasesMiceMice, Inbred C57BLObesityRNA, MessengerRNA, Messenger

Identifiers

PMID34663892
PMCPMC8794789
OpenAlexW3206325051

What OpenQuestion holds

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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.