Evidence map›Paper›PMID 24692138›Full record

ReviewComprehensive Physiology2014

Energy metabolism in the liver.

Liangyou Rui

Abstract readReview
In one paragraph

Review in Comprehensive Physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,133 papers.

0numbers the graph read from it
0cells of the map it votes in
1,133citing papers in PubMed
–field-weighted citation impact
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

1,133 citing papers in PubMed, 1,961 citations in OpenAlex.

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  15. Vanadium(IV)-chlorodipicolinate alleviates hepatic steatosis via the AMPK/PGC-1α/CPT1a axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
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1,073 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

1 author at 1 institution in 1 country.

Liangyou RuiDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan.
University of Michigan–Ann Arbor · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Role of SH2-B in Glucose MetabolismR01DK065122 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2004 to 2012
$2.9M
Transcriptional Regulation of MetabolismR01DK094014 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2012 to 2015
$1.5M
Role of inflammation and cellular stress in the pathogenesis of type 2 diabetesR01DK091591 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2012 to 2015
$1.5M
NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK 065122NIDDK NIH HHS R01 DK065122NIDDK NIH HHS R01 DK091591NIDDK NIH HHS R01 DK094014
6 · The paper itself

Abstract

The liver is an essential metabolic organ, and its metabolic function is controlled by insulin and other metabolic hormones. Glucose is converted into pyruvate through glycolysis in the cytoplasm, and pyruvate is subsequently oxidized in the mitochondria to generate ATP through the TCA cycle and oxidative phosphorylation. In the fed state, glycolytic products are used to synthesize fatty acids through de novo lipogenesis. Long-chain fatty acids are incorporated into triacylglycerol, phospholipids, and/or cholesterol esters in hepatocytes. These complex lipids are stored in lipid droplets and membrane structures, or secreted into the circulation as very low-density lipoprotein particles. In the fasted state, the liver secretes glucose through both glycogenolysis and gluconeogenesis. During pronged fasting, hepatic gluconeogenesis is the primary source for endogenous glucose production. Fasting also promotes lipolysis in adipose tissue, resulting in release of nonesterified fatty acids which are converted into ketone bodies in hepatic mitochondria though β-oxidation and ketogenesis. Ketone bodies provide a metabolic fuel for extrahepatic tissues. Liver energy metabolism is tightly regulated by neuronal and hormonal signals. The sympathetic system stimulates, whereas the parasympathetic system suppresses, hepatic gluconeogenesis. Insulin stimulates glycolysis and lipogenesis but suppresses gluconeogenesis, and glucagon counteracts insulin action. Numerous transcription factors and coactivators, including CREB, FOXO1, ChREBP, SREBP, PGC-1α, and CRTC2, control the expression of the enzymes which catalyze key steps of metabolic pathways, thus controlling liver energy metabolism. Aberrant energy metabolism in the liver promotes insulin resistance, diabetes, and nonalcoholic fatty liver diseases.

Indexed as

Circadian RhythmCytokinesDiabetes Mellitus, Type 2Endoplasmic ReticulumEnergy MetabolismFatty AcidsGlucagonGluconeogenesisGlucoseHuman Growth HormoneHumansInsulinLipogenesisLiverNon-alcoholic Fatty Liver DiseaseObesityCytokinesFatty AcidsGlucagonGlucoseHuman Growth HormoneInsulin

Identifiers

PMID24692138
PMCPMC4050641
OpenAlexW1503760388

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.