Evidence map›Paper›PMID 31918925›Full record

ArticleMolecular metabolism2020

FDG uptake tracks the oxidative damage in diabetic skeletal muscle: An experimental study.

Matteo Bauckneht, Vanessa Cossu, Patrizia Castellani, Patrizia Piccioli, Anna Maria Orengo, Laura Emionite, Francesco Di Giulio, Maria Isabella Donegani, Alberto Miceli, Stefano Raffa and 9 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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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

19 authors at 3 institutions in 1 country.

Matteo BaucknehtNuclear Medicine, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy; Department of Health Sciences, University of Genoa, Via Pastore 1, 16132 Genoa, Italy.
Vanessa CossuNuclear Medicine, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy; Department of Health Sciences, University of Genoa, Via Pastore 1, 16132 Genoa, Italy.
Patrizia CastellaniCell Biology Unit, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy.
Patrizia PiccioliCell Biology Unit, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy.
Anna Maria OrengoNuclear Medicine, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy.
Laura EmioniteAnimal Facility, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy.
Francesco Di GiulioNuclear Medicine, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy.
Maria Isabella DoneganiDepartment of Health Sciences, University of Genoa, Via Pastore 1, 16132 Genoa, Italy.
Alberto MiceliDepartment of Health Sciences, University of Genoa, Via Pastore 1, 16132 Genoa, Italy.
Stefano RaffaDepartment of Health Sciences, University of Genoa, Via Pastore 1, 16132 Genoa, Italy.
Anna BorraDepartment of Health Sciences, University of Genoa, Via Pastore 1, 16132 Genoa, Italy.
Selene CapitanioNuclear Medicine, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy.
Silvia MorbelliNuclear Medicine, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy; Department of Health Sciences, University of Genoa, Via Pastore 1, 16132 Genoa, Italy.
Giacomo CavigliaDepartment Experimental Medicine, University of Genoa, Len Battista Alberti 2, 16132 Genoa, Italy.
Silvia BrunoDepartment of Internal Medicine, University of Genoa, Viale Benedetto XV 6, 16132 Genoa, Italy.
Silvia RaveraDepartment of Internal Medicine, University of Genoa, Viale Benedetto XV 6, 16132 Genoa, Italy.
Davide MaggiDiabetes Unit, IRCCS Ospedale Policlinico San Martino Genoa, Largo Benzi 10, 16132 Genoa, Italy; Department of Mathematics (DIMA), University of Genoa, Via Dodecaneso 35, 16146 Genoa, Italy.
Gianmario SambucetiNuclear Medicine, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy; Department of Health Sciences, University of Genoa, Via Pastore 1, 16132 Genoa, Italy.
Cecilia MariniNuclear Medicine, IRCCS Ospedale Policlinico San Martino, Largo Benzi 10, 16132 Genoa, Italy; CNR Institute of Molecular Bioimaging and Physiology (IBFM), Via Fratelli Cervi 93, 20090 Segrate (MI), Italy. Electronic address: cecilia.marini@unige.it.
Ospedale Policlinico San Martino · ITUniversity of Genoa · ITInstitute of Molecular Bioimaging and Physiology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe present study aims to verify the relationship between glucose consumption and uptake of

methodsThe study included 36 Balb/c mice. Two weeks after intraperitoneal administration of saline (control group, n = 18) or 150 mg streptozotocin (STZ-DM group, n = 18), the two cohorts were submitted to an oral glucose tolerance test and were further subdivided into three groups (n = 6 each): untreated and treated with metformin (MTF) at low or high doses (10 or 750 mg/kg daily, respectively). Two weeks thereafter, all mice were submitted to dynamic micro-positron emission tomography (PET) imaging after prolonged fasting. After sacrifice, enzymatic pathways and response to oxidative stress were evaluated in harvested SM.

resultsOn PET imaging, the FDG uptake rate in hindlimb SM was significantly lower in nondiabetic mice as compared with STZ-DM-untreated mice. MTF had no significant effect on SM FDG uptake in untreated mice; however, its high dose induced a significant decrease in STZ-DM animals. Upon conventional analysis, the SM standard uptake value was higher in STZ-DM mice, while MTF was virtually ineffective in either control or STZ-DM models. This metabolic reprogramming was not explained by any change in cytosolic glucose metabolism. By contrast, it closely agreed with the catalytic function of hexose-6P-dehydrogenase (H6PD; i.e., the trigger of a specific pentose phosphate pathway selectively located within the endoplasmic reticulum). In agreement with this role, the H6PD enzymatic response to both STZ-DM and MTF matched the activation of the NADPH-dependent antioxidant responses to the increased generation of reactive oxygen species caused by chronic hyperglycemia. Ex vivo analysis of tracer kinetics confirmed that the enhanced SM avidity for FDG occurred despite a significant reduction in glucose consumption, while it was associated with increased radioactivity transfer to the endoplasmic reticulum.

conclusionsThese data challenge the current dogma linking FDG uptake to the glycolytic rate. They instead introduce a new model considering a strict link between the uptake of this glucose analog, H6PD reticular activity, and oxidative damage in diabetes, at least under fasting condition.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalFastingFluorodeoxyglucose F18Glucose Tolerance TestInjections, IntraperitonealMaleMiceMice, Inbred BALB CMuscle, SkeletalOxidative StressPositron-Emission TomographyStreptozocinFluorodeoxyglucose F18StreptozocinDiabetesFluorodeoxyglucoseHexose-6P-dehydrogenaseOxidative stressSkeletal muscle

Identifiers

PMID31918925
PMCPMC6920267
OpenAlexW2985115016

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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.