Evidence map›Paper›PMID 30034573›Full record

ReviewOxidative medicine and cellular longevity2018

mTOR Inhibitor Therapy and Metabolic Consequences: Where Do We Stand?

Aleksandra Kezic, Ljiljana Popovic, Katarina Lalic

Open access · hybridFull text readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 62 citations in OpenAlex.

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  7. Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026
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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

3 authors at 1 institution in 1 country.

Aleksandra KezicFaculty of Medicine, University of Belgrade, Dr Subotica 8, 11000 Belgrade, Serbia.ORCID 0000-0003-1790-7955
Ljiljana PopovicFaculty of Medicine, University of Belgrade, Dr Subotica 8, 11000 Belgrade, Serbia.
Katarina LalicFaculty of Medicine, University of Belgrade, Dr Subotica 8, 11000 Belgrade, Serbia.ORCID 0000-0002-8070-1899
University of Belgrade · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

mTOR (mechanistic target of rapamycin) protein kinase acts as a central integrator of nutrient signaling pathways. Besides the immunosuppressive role after solid organ transplantations or in the treatment of some cancers, another promising role of mTOR inhibitor as an antiaging therapeutic has emerged in the recent years. Acute or intermittent rapamycin treatment has some resemblance to calorie restriction in metabolic effects such as an increased insulin sensitivity. However, the chronic inhibition of mTOR by macrolide rapamycin or other rapalogs has been associated with glucose intolerance and insulin resistance and may even provoke type II diabetes. These metabolic adverse effects limit the use of mTOR inhibitors. Metformin is a widely used drug for the treatment of type 2 diabetes which activates AMP-activated protein kinase (AMPK), acting as calorie restriction mimetic. In addition to the glucose-lowering effect resulting from the decreased hepatic glucose production and increased glucose utilization, metformin induces fatty acid oxidations. Here, we review the recent advances in our understanding of the metabolic consequences regarding glucose metabolism induced by mTOR inhibitors and compare them to the metabolic profile provoked by metformin use. We further suggest metformin use concurrent with rapalogs in order to pharmacologically address the impaired glucose metabolism and prevent the development of new-onset diabetes mellitus after solid organ transplantations induced by the chronic rapalog treatment.

Indexed as

AMP-Activated Protein KinasesAnimalsDiabetes Mellitus, Type 2GlucoseHumansMetforminTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlucoseMetforminTOR Serine-Threonine Kinases

Identifiers

PMID30034573
PMCPMC6035806
OpenAlexW2809753616

What Socratic holds

Textfull text, public
LicenceCC BY
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 Socratic graph.