Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion Imbalance

Second-generation antipsychotics (SGAs) are known to increase cardiovascular risk through several physiological mechanisms, including insulin resistance, hepatic steatosis, hyperphagia, and accelerated weight gain. There are limited prophylactic interventions to prevent these side effects of SGAs, i...

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Main Authors: Andrea del Campo, Catalina Bustos, Carolina Mascayano, Claudio Acuña-Castillo, Rodrigo Troncoso, Leonel E. Rojo
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-04-01
Series:Frontiers in Endocrinology
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fendo.2018.00144/full
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author Andrea del Campo
Andrea del Campo
Andrea del Campo
Catalina Bustos
Carolina Mascayano
Claudio Acuña-Castillo
Claudio Acuña-Castillo
Rodrigo Troncoso
Leonel E. Rojo
Leonel E. Rojo
author_facet Andrea del Campo
Andrea del Campo
Andrea del Campo
Catalina Bustos
Carolina Mascayano
Claudio Acuña-Castillo
Claudio Acuña-Castillo
Rodrigo Troncoso
Leonel E. Rojo
Leonel E. Rojo
author_sort Andrea del Campo
collection DOAJ
description Second-generation antipsychotics (SGAs) are known to increase cardiovascular risk through several physiological mechanisms, including insulin resistance, hepatic steatosis, hyperphagia, and accelerated weight gain. There are limited prophylactic interventions to prevent these side effects of SGAs, in part because the molecular mechanisms underlying SGAs toxicity are not yet completely elucidated. In this perspective article, we introduce an innovative approach to study the metabolic side effects of antipsychotics through the alterations of the mitochondrial dynamics, which leads to an imbalance in mitochondrial fusion/fission ratio and to an inefficient mitochondrial phenotype of muscle cells. We believe that this approach may offer a valuable path to explain SGAs-induced alterations in metabolic homeostasis.
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spelling doaj.art-39b07853024348e3914181144796d1b32022-12-21T22:21:53ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922018-04-01910.3389/fendo.2018.00144316281Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion ImbalanceAndrea del Campo0Andrea del Campo1Andrea del Campo2Catalina Bustos3Carolina Mascayano4Claudio Acuña-Castillo5Claudio Acuña-Castillo6Rodrigo Troncoso7Leonel E. Rojo8Leonel E. Rojo9Departamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, ChileEscuela de Química y Farmacia, Facultad de Ingeniería, Ciencia y Tecnología, Universidad Bernardo O’Higgins, Santiago, ChilePrograma de Biología Celular y Molecular, Facultad de Medicina, Universidad de Chile, Santiago, ChileDepartamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, ChileDepartamento de Ciencias del Ambiente, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, ChileDepartamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, ChileCentro de Biotecnología Acuícola, Universidad de Santiago de Chile, Santiago, ChileLaboratorio de Investigación en Nutrición y Actividad Física, Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, ChileDepartamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, ChileCentro de Biotecnología Acuícola, Universidad de Santiago de Chile, Santiago, ChileSecond-generation antipsychotics (SGAs) are known to increase cardiovascular risk through several physiological mechanisms, including insulin resistance, hepatic steatosis, hyperphagia, and accelerated weight gain. There are limited prophylactic interventions to prevent these side effects of SGAs, in part because the molecular mechanisms underlying SGAs toxicity are not yet completely elucidated. In this perspective article, we introduce an innovative approach to study the metabolic side effects of antipsychotics through the alterations of the mitochondrial dynamics, which leads to an imbalance in mitochondrial fusion/fission ratio and to an inefficient mitochondrial phenotype of muscle cells. We believe that this approach may offer a valuable path to explain SGAs-induced alterations in metabolic homeostasis.http://journal.frontiersin.org/article/10.3389/fendo.2018.00144/fullsecond-generation antipsychotic agentsmitochondrial dynamicsinsulin resistanceL6 muscle cellsobesity
spellingShingle Andrea del Campo
Andrea del Campo
Andrea del Campo
Catalina Bustos
Carolina Mascayano
Claudio Acuña-Castillo
Claudio Acuña-Castillo
Rodrigo Troncoso
Leonel E. Rojo
Leonel E. Rojo
Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion Imbalance
Frontiers in Endocrinology
second-generation antipsychotic agents
mitochondrial dynamics
insulin resistance
L6 muscle cells
obesity
title Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion Imbalance
title_full Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion Imbalance
title_fullStr Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion Imbalance
title_full_unstemmed Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion Imbalance
title_short Metabolic Syndrome and Antipsychotics: The Role of Mitochondrial Fission/Fusion Imbalance
title_sort metabolic syndrome and antipsychotics the role of mitochondrial fission fusion imbalance
topic second-generation antipsychotic agents
mitochondrial dynamics
insulin resistance
L6 muscle cells
obesity
url http://journal.frontiersin.org/article/10.3389/fendo.2018.00144/full
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