Evidence map›Paper›PMID 30841536›Full record

ReviewInternational journal of molecular sciences2019

mTOR is a Key Protein Involved in the Metabolic Effects of Simple Sugars.

Gemma Sangüesa, Núria Roglans, Miguel Baena, Ana Magdalena Velázquez, Juan Carlos Laguna, Marta Alegret

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  15. Dietary intake of fructose increases purineFrontiers in nutrition · 2022
    Article
  16. Article
  17. Article
  18. Frontiers in physiology · 2021
    Review
  19. Article
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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

6 authors at 3 institutions in 1 country.

Gemma SangüesaDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, School of Pharmacy and Food Science, University of Barcelona, 08028 Barcelona, Spain. gemmasanguesa@gmail.com.ORCID 0000-0002-6902-4372
Núria RoglansDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, School of Pharmacy and Food Science, University of Barcelona, 08028 Barcelona, Spain. roglans@ub.edu.
Miguel BaenaDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, School of Pharmacy and Food Science, University of Barcelona, 08028 Barcelona, Spain. mbaena@uic.es.
Ana Magdalena VelázquezDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, School of Pharmacy and Food Science, University of Barcelona, 08028 Barcelona, Spain. avelazquezpy@gmail.com.
Juan Carlos LagunaDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, School of Pharmacy and Food Science, University of Barcelona, 08028 Barcelona, Spain. jclagunae@ub.edu.
Marta AlegretDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, School of Pharmacy and Food Science, University of Barcelona, 08028 Barcelona, Spain. alegret@ub.edu.ORCID 0000-0002-5652-8651
Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition · ESInstitute for Research in Biomedicine · ESUniversitat de Barcelona · ES

Funding

Generalitat de Catalunya SGR09-00413; SGR13-00066 and 2017 SGR 38Ministerio de Economía, Industria y Competitividad, Gobierno de España SAF2010-15664, SAF2013-42982-R and SAF2017-82369-R
6 · The paper itself

Abstract

One of the most important threats to global human health is the increasing incidences of metabolic pathologies (including obesity, type 2 diabetes and non-alcoholic fatty liver disease), which is paralleled by increasing consumptions of hypercaloric diets enriched in simple sugars. The challenge is to identify the metabolic pathways affected by the excessive consumption of these dietary components when they are consumed in excess, to unravel the molecular mechanisms leading to metabolic pathologies and identify novel therapeutic targets to manage them. Mechanistic (mammalian) target of rapamycin (mTOR) has emerged as one of the key molecular nodes that integrate extracellular signals, such as energy status and nutrient availability, to trigger cell responses that could lead to the above-mentioned diseases through the regulation of lipid and glucose metabolism. By activating mTOR signalling, excessive consumption of simple sugars (such as fructose and glucose), could modulate hepatic gluconeogenesis, lipogenesis and fatty acid uptake and catabolism and thus lipid deposition in the liver. In the present review we will discuss some of the most recent studies showing the central role of mTOR in the metabolic effects of excessive simple sugar consumption.

Indexed as

AnimalsFructoseGlucoseHumansLipid MetabolismLiverSignal TransductionTOR Serine-Threonine KinasesFructoseGlucoseTOR Serine-Threonine Kinasesfructosegluconeogenesisglucoselipid metabolismlivermTOR

Identifiers

PMID30841536
PMCPMC6429387
OpenAlexW2919098381

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.