Evidence map›Paper›PMID 12920182›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Acetyl-CoA carboxylase 2 mutant mice are protected against obesity and diabetes induced by high-fat/high-carbohydrate diets.

Lutfi Abu-Elheiga, Wonkeun Oh, Parichher Kordari, Salih J Wakil

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed
14.3field-weighted citation impact, top 1% 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

131 citing papers in PubMed, 385 citations in OpenAlex.

  1. Trial
  2. Local Suppression ofJournal of microbiology and biotechnology · 2026
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  13. Atherosclerosis Impairs Naive CD4 T-Cell Responses via Disruption of Glycolysis.Arteriosclerosis, thrombosis, and vascular biology · 2021
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71 more citing papers are in PubMed but not listed here.

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.

Lutfi Abu-ElheigaVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Wonkeun Oh
Parichher Kordari
Salih J Wakil
Baylor College of Medicine · US

Funding

Role of the Acetyl-CoA Carboxylases in Energy MetabolismR01GM063115 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI WAKIL, SALIH JAWAD · 2002 to 2011
$3.2M
NIGMS NIH HHS GM-63115NIGMS NIH HHS R01 GM063115
6 · The paper itself

Abstract

Malonyl-CoA, generated by acetyl-CoA carboxylases ACC1 and ACC2, is a key metabolite in the control of fatty acid synthesis and oxidation in response to dietary changes. ACC2 is associated to the mitochondria, and Acc2-/- mice have a normal lifespan and higher fatty acid oxidation rate and accumulate less fat. Mutant mice fed high-fat/high-carbohydrate diets weighed less than their WT cohorts, accumulated less fat, and maintained normal levels of insulin and glucose, whereas the WT mice became type-2 diabetic with hyperglycemic and hyperinsulinemic status. Fatty acid oxidation rates in the soleus muscle and in hepatocytes of Acc2-/- mice were significantly higher than those of WT cohorts and were not affected by the addition of insulin. mRNA levels of uncoupling proteins (UCPs) were significantly higher in adipose, heart (UCP2), and muscle (UCP3) tissues of mutant mice compared with those of the WT. The increase in the UCP levels along with increased fatty acid oxidation may play an essential role in the regulation of energy expenditure. Lowering intracellular fatty acid accumulation in the mutant relative to that of the WT mice may thus impact glucose transport by higher GLUT4 activity and insulin sensitivity. These results suggest that ACC2 plays an essential role in controlling fatty acid oxidation and is a potential target in therapy against obesity and related diseases.

Indexed as

Membrane Transport ProteinsMitochondrial ProteinsAcetyl-CoA CarboxylaseAnimalsCarrier ProteinsDiabetes Mellitus, Type 2Dietary CarbohydratesDietary FatsFatty AcidsFemaleGlucose Tolerance TestHepatocytesInsulinIon ChannelsMaleMiceAcetyl-CoA CarboxylaseCarrier ProteinsDietary CarbohydratesDietary FatsFatty AcidsInsulinIon ChannelsMembrane Transport ProteinsMitochondrial ProteinsProteinsUcp2 protein, mouseUcp3 protein, mouseUncoupling Protein 2Uncoupling Protein 3

Identifiers

PMID12920182
PMCPMC193540
OpenAlexW2065034018

What OpenQuestion holds

Textmetadata
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.