Evidence map›Paper›PMID 31671770›Full record

ReviewCells2019

Second-Generation Antipsychotics and Dysregulation of Glucose Metabolism: Beyond Weight Gain.

Diana Grajales, Vitor Ferreira, Ángela M Valverde

Abstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 3 pooled it
–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

91 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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31 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

3 authors.

Diana GrajalesInstituto de Investigaciones Biomédicas Alberto Sols (CSIC-UAM), 28029 Madrid, Spain. dgrajales@iib.uam.es.ORCID 0000-0002-9332-6979
Vitor FerreiraInstituto de Investigaciones Biomédicas Alberto Sols (CSIC-UAM), 28029 Madrid, Spain. vdasilva@iib.uam.es.
Ángela M ValverdeInstituto de Investigaciones Biomédicas Alberto Sols (CSIC-UAM), 28029 Madrid, Spain. avalverde@iib.uam.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Second-generation antipsychotics (SGAs) are the cornerstone of treatment for schizophrenia because of their high clinical efficacy. However, SGA treatment is associated with severe metabolic alterations and body weight gain, which can increase the risk of type 2 diabetes and cardiovascular disease, and greatly accelerate mortality. Several underlying mechanisms have been proposed for antipsychotic-induced weight gain (AIWG), but some studies suggest that metabolic changes in insulin-sensitive tissues can be triggered before the onset of AIWG. In this review, we give an outlook on current research about the metabolic disturbances provoked by SGAs, with a particular focus on whole-body glucose homeostasis disturbances induced independently of AIWG, lipid dysregulation or adipose tissue disturbances. Specifically, we discuss the mechanistic insights gleamed from cellular and preclinical animal studies that have reported on the impact of SGAs on insulin signaling, endogenous glucose production, glucose uptake and insulin secretion in the liver, skeletal muscle and the endocrine pancreas. Finally, we discuss some of the genetic and epigenetic changes that might explain the different susceptibilities of SGA-treated patients to the metabolic side-effects of antipsychotics.

Indexed as

Adipose TissueAnimalsAntipsychotic AgentsDiabetes Mellitus, Type 2GlucoseGlucose Metabolism DisordersHomeostasisHumansInsulinSchizophreniaWeight GainAntipsychotic AgentsGlucoseInsulinantipsychoticsglucose dysregulationinsulin resistanceinsulin secretionmetabolic side-effectsschizophreniasecond-generation antipsychoticstype 2 diabetes

Identifiers

PMID31671770
PMCPMC6912706

What OpenQuestion holds

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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.