Evidence map›Paper›PMID 25511531›Full record

ArticleBMC endocrine disorders2014

AMPD1: a novel therapeutic target for reversing insulin resistance.

Jidong Cheng, Hiroko Morisaki, Keiko Toyama, Naomi Sugimoto, Takuya Shintani, Andreas Tandelilin, Tetsuaki Hirase, Edward W Holmes, Takayuki Morisaki

Open access · goldAbstract read
In one paragraph

Article in BMC endocrine disorders, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Role of AMP deaminase in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024
    Review
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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

9 authors at 3 institutions in 3 countries.

Jidong Cheng
Hiroko Morisaki
Keiko Toyama
Naomi Sugimoto
Takuya Shintani
Andreas Tandelilin
Tetsuaki Hirase
Edward W Holmes
Takayuki MorisakiDepartment of Bioscience and Genetics, National Cerebral and Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan. morisaki@ri.ncvc.go.jp.
National Cerebral and Cardiovascular Center · JPOsaka University · JPSanford Consortium for Regenerative Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin resistance is one of the hallmark manifestations of obesity and Type II diabetes and reversal of this pathogenic abnormality is an attractive target for new therapies for Type II diabetes. A recent report that metformin, a drug known to reverse insulin resistance, demonstrated in vitro the metformin can inhibit AMP deaminase (AMPD) activity. Skeletal muscle is one of the primary organs contributing to insulin resistance and that the AMPD1 gene is selectively expressed at high levels in skeletal muscle.

methodsRecognizing the background above, we asked if genetic disruption of the AMPD1 gene might ameliorate the manifestations of insulin resistance. AMPD1 deficient homozygous mice and control mice fed normal chow diet or a high-fat diet, and blood analysis, glucose tolerance test and insulin tolerance test were performed. Also, skeletal muscle metabolism and gene expression including nucleotide levels and activation of AMP activated protein kinase (AMP kinase) were evaluated in both conditions.

resultsDisruption of the AMPD1 gene leads to a less severe state of insulin resistance, improved glucose tolerance and enhanced insulin clearance in mice fed a high fat diet. Given the central role of AMP kinase in insulin action, and its response to changes in AMP concentrations in the cell, we examined the skeletal muscle of the AMPD1 deficient mice and found that they have greater AMP kinase activity as evidenced by higher levels of phosphorylated AMP kinase.

conclusionsTaken together these data suggest that AMPD may be a new drug target for the reversal of insulin resistance and the treatment of Type II diabetes.

Indexed as

Insulin ResistanceAMP-Activated Protein KinasesAMP DeaminaseAnimalsBlood GlucoseDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalGene Expression RegulationMiceMice, Inbred C57BLMice, TransgenicMuscle, SkeletalObesityAMP-Activated Protein KinasesAMPD1 protein, mouseAMP DeaminaseBlood Glucose

Identifiers

PMID25511531
PMCPMC4274759
OpenAlexW1619199252

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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.