Evidence map›Paper›PMID 31630081›Full record

ArticleThe Journal of nutritional biochemistry2019

Role of microRNA-122 in hepatic lipid metabolism of the weanling female rat offspring exposed to prenatal and postnatal caloric restriction.

Yun Dai, Shubhamoy Ghosh, Bo-Chul Shin, Sherin U Devaskar

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of nutritional biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Correlation analysis of the impact ofMicrobiology spectrum · 2025
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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

4 authors at 1 institution in 1 country.

Yun DaiDepartment of Pediatrics and the Children's Discovery and Innovation Institute, David Geffen School of Medicine UCLA, Los Angeles, CA.
Shubhamoy GhoshDepartment of Pediatrics and the Children's Discovery and Innovation Institute, David Geffen School of Medicine UCLA, Los Angeles, CA.
Bo-Chul ShinDepartment of Pediatrics and the Children's Discovery and Innovation Institute, David Geffen School of Medicine UCLA, Los Angeles, CA.
Sherin U DevaskarDepartment of Pediatrics and the Children's Discovery and Innovation Institute, David Geffen School of Medicine UCLA, Los Angeles, CA. Electronic address: sdevaskar@mednet.ucla.edu.
Children’s Institute · US

Funding

Prenatal Metabolic Programming of the OffspringR01HD041230 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2001 to 2019
$5.2M
Prenatal Origins of Neurometabolic ConsequencesR01HD081206 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2015 to 2024
$4.1M
NICHD NIH HHS R01 HD041230NICHD NIH HHS R01 HD081206
6 · The paper itself

Abstract

We examined the role of hepatocyte micro-RNA-122 and hypothalamic neuropeptides, in weanling (21d) female rats exposed to calorie restriction induced growth restriction either prenatally (IUGR), postnatally (PNGR) or both (IPGR) vs. ad lib fed controls (CON). IUGR were hyperinsulinemic, hyperleptinemic and dyslipidemic with high circulating miR-122. In contrast, PNGR and IPGR displayed insufficient glucose, insulin and leptin amidst high ketones with a dichotomy in circulating miR-122 of PNGR<IPGR = CON. Examination of livers revealed a reduction in miR-122 expression in PNGR and IPGR reflecting the hepatic size. This reduction of hepatic miR-122 was associated with an increase in specific target transcripts (ALDO-A, BCKDK, PPAR-β) and those mediating fatty acid oxidation (PGC-1α, CPT-1α), with a concomitant suppression of fatty acid and cholesterol synthesizing transcripts (FAS, HMGCR). Functionally, these changes correlated with increased fatty acid oxidation and mitochondrial CPT1α enzyme activity ex vivo. In vitro physiologic (serum starvation) and genetic manipulation of miR-122 in H4IIE hepatoma cells revealed fidelity in regulating ALDO-A/BCKDK, but an infidelity in perturbing fatty acid/cholesterol synthesizing and oxidizing gene transcripts. Nevertheless, changes in endogenous miR-122 maintained singular directionality while altering FAS/HMGCR and CPT-1α/PGC-1α, almost reflecting each other, and thereby maintaining a balance in fatty acid/cholesterol supply necessary to meet the in vitro demands of these rapidly proliferating transformed cells. Successive microarray based analysis, comparing IPGR to CON demonstrated differential expression of hypothalamic genes mediating cell proliferation and survival, appetite/energy balance, circadian rhythm and obesity/diabetes. We conclude that miR-122 regulates genes mediating fatty acid/cholesterol metabolism in postnatal female rats, fueling the energy demand.

Indexed as

AnimalsBody WeightCaloric RestrictionCircadian RhythmEnergy MetabolismFatty AcidsFemaleFetal Growth RetardationGene ExpressionGrowth DisordersHypothalamusLipid MetabolismLiverMicroRNAsOrgan SizePregnancyFatty AcidsMicroRNAsMIRN122 microRNA, ratRNA, MessengerCircadian rhythmEnergy balanceFatty acid oxidationHepatic fatty acid synthesisHypothalamic genesIntra-uterine growth restrictionmicroRNA-122

Identifiers

PMID31630081
PMCPMC6896790
OpenAlexW2968353691

What OpenQuestion holds

Textmetadata
LicenceTDM
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.