Evidence map›Paper›PMID 32113910›Full record

ReviewRedox biology2020

Lactate as a fulcrum of metabolism.

George A Brooks

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 423 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
423citing papers in PubMed, 1 pooled it
35.4field-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

423 citing papers in PubMed, 1 synthesis or guideline pooled it, 676 citations in OpenAlex.

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363 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.

George A BrooksExercise Physiology Laboratory, Department of Integrative Biology, University of California, Berkeley, CA, 94720-3140, USA. Electronic address: gbrooks@berkeley.edu.
University of California, Berkeley · US

Funding

Aging Mitochondrial Fragmentation and Metabolic InflexibilityR01AG059715 · NIA · UNIVERSITY OF CALIFORNIA BERKELEY · PI BROOKS, GEORGE AUSTIN · 2018 to 2022
$3.0M
NIA NIH HHS R01 AG059715
6 · The paper itself

Abstract

Mistakenly thought to be the consequence of oxygen lack in contracting skeletal muscle we now know that the L-enantiomer of the lactate anion is formed under fully aerobic conditions and is utilized continuously in diverse cells, tissues, organs and at the whole-body level. By shuttling between producer (driver) and consumer (recipient) cells lactate fulfills at least three purposes: 1] a major energy source for mitochondrial respiration; 2] the major gluconeogenic precursor; and 3] a signaling molecule. Working by mass action, cell redox regulation, allosteric binding, and reprogramming of chromatin by lactylation of lysine residues on histones, lactate has major influences in energy substrate partitioning. The physiological range of tissue [lactate] is 0.5-20 mM and the cellular Lactate/Pyruvate ratio (L/P) can range from 10 to >500; these changes during exercise and other stress-strain responses dwarf other metabolic signals in magnitude and span. Hence, lactate dynamics have rapid and major short- and long-term effects on cell redox and other control systems. By inhibiting lipolysis in adipose via HCAR-1, and muscle mitochondrial fatty acid uptake via malonyl-CoA and CPT1, lactate controls energy substrate partitioning. Repeated lactate exposure from regular exercise results in major effects on the expression of regulatory enzymes of glycolysis and mitochondrial respiration. Lactate is the fulcrum of metabolic regulation in vivo.

Indexed as

GlycolysisLactic AcidEnergy MetabolismMitochondriaMuscle, SkeletalOxidation-ReductionLactic AcidAerobicAnaerobicCell-cell signalingEnergy substrate partitioningExerciseGluconeogenesisGlycolysisHCAR1Histone lactylationMitochondrial biogenesisOxidative metabolismPGC-1αPPAR-γSIRT activationTGFβ

Identifiers

PMID32113910
PMCPMC7284908
OpenAlexW3005469631

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.