Evidence map›Paper›PMID 33667544›Full record

ArticleThe Journal of biological chemistry

Increasing hepatic glycogen moderates the diabetic phenotype in insulin-deficient Akita mice.

Iliana López-Soldado, Joan J Guinovart, Jordi Duran

Open access · goldAbstract read
In one paragraph

Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Peel of Pomegranate Fruit (Current issues in molecular biology · 2026
    Article
  2. Twelve weeks of voluntary wheel running restores glucagon sensitivity in middle-aged mice.American journal of physiology. Endocrinology and metabolism · 2026
    Article
  3. Article
  4. Article
  5. Hypoglycemic and hypolipidemic effect of pentaamino acid fullerene CJournal of bioenergetics and biomembranes · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. 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

3 authors at 2 institutions in 1 country.

Iliana López-SoldadoInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, Spain. Electronic address: iliana.lopez@irbbarcelona.org.
Joan J GuinovartInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, Spain; Department of Biochemistry and Molecular Biomedicine, University of Barcelona, Barcelona, Spain.
Jordi DuranInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, Spain.
Institute for Research in Biomedicine · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic glycogen metabolism is impaired in diabetes. We previously demonstrated that strategies to increase liver glycogen content in a high-fat-diet mouse model of obesity and insulin resistance led to a reduction in food intake and ameliorated obesity and glucose tolerance. These effects were accompanied by a decrease in insulin levels, but whether this decrease contributed to the phenotype observed in this animal was unclear. Here we sought to evaluate this aspect directly, by examining the long-term effects of increasing liver glycogen in an animal model of insulin-deficient and monogenic diabetes, namely the Akita mouse, which is characterized by reduced insulin production. We crossed Akita mice with animals overexpressing protein targeting to glycogen (PTG) in the liver to generate Akita mice with increased liver glycogen content (Akita-PTG

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalFemaleGluconeogenesisGlycolysisInsulinIntracellular Signaling Peptides and ProteinsLiver GlycogenMaleMiceMice, Inbred C57BLPhenotypeInsulinIntracellular Signaling Peptides and ProteinsLiver GlycogenPpp1r3c protein, mouseAkitaATPdiabetesgluconeogenesisglucoseglycogenglycolysisinsulinliverprotein targeting to glycogen (PTG)

Identifiers

PMID33667544
PMCPMC8027280
OpenAlexW3135295609

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.