Evidence map›Paper›PMID 19245656›Full record

ReviewActa physiologica (Oxford, England)2009

AMP-activated protein kinase in the regulation of hepatic energy metabolism: from physiology to therapeutic perspectives.

B Viollet, B Guigas, J Leclerc, S Hébrard, L Lantier, R Mounier, F Andreelli, M Foretz

Open access · greenAbstract readReview
In one paragraph

Review in Acta physiologica (Oxford, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 205 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
205citing papers in PubMed, 1 pooled it
11.2field-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

205 citing papers in PubMed, 1 synthesis or guideline pooled it, 480 citations in OpenAlex.

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145 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

8 authors at 4 institutions in 3 countries.

B ViolletDepartment of Endocrinology, Metabolism and Cancer, Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), 24 rue du Faubourg Saint-Jacques, Paris, France. benoit.viollet@inserm.fr
B Guigas
J Leclerc
S Hébrard
L Lantier
R Mounier
F Andreelli
M Foretz
Centre National de la Recherche Scientifique · FRInserm · FRLeiden University Medical Center · NLUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the liver is central in the maintenance of glucose homeostasis and energy storage, knowledge of the physiology as well as physiopathology of hepatic energy metabolism is a prerequisite to our understanding of whole-body metabolism. Hepatic fuel metabolism changes considerably depending on physiological circumstances (fed vs. fasted state). In consequence, hepatic carbohydrate, lipid and protein synthesis/utilization are tightly regulated according to needs. Fatty liver and hepatic insulin resistance (both frequently associated with the metabolic syndrome) or increased hepatic glucose production (as observed in type 2 diabetes) resulted from alterations in substrates oxidation/storage balance in the liver. Because AMP-activated protein kinase (AMPK) is considered as a cellular energy sensor, it is important to gain understanding of the mechanism by which hepatic AMPK coordinates hepatic energy metabolism. AMPK has been implicated as a key regulator of physiological energy dynamics by limiting anabolic pathways (to prevent further ATP consumption) and by facilitating catabolic pathways (to increase ATP generation). Activation of hepatic AMPK leads to increased fatty acid oxidation and simultaneously inhibition of hepatic lipogenesis, cholesterol synthesis and glucose production. In addition to a short-term effect on specific enzymes, AMPK also modulates the transcription of genes involved in lipogenesis and mitochondrial biogenesis. The identification of AMPK targets in hepatic metabolism should be useful in developing treatments to reverse metabolic abnormalities of type 2 diabetes and the metabolic syndrome.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsDyslipidemiasEnergy MetabolismFatty LiverGluconeogenesisGlucoseHomeostasisHumansHypoglycemic AgentsLipid MetabolismLiverLiver CirrhosisMitochondriaProtein ConformationAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesGlucoseHypoglycemic AgentsProtein SubunitsRibonucleotides

Identifiers

PMID19245656
PMCPMC2956117
OpenAlexW1995501935

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.