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Mitochondrial targets of metformin-Are they physiologically relevant?
Pecinová, Alena; Brázdová, Andrea; Drahota, Zdenek; Houstek, Josef; Mrácek, Tomás.
Afiliação
  • Pecinová A; Department of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
  • Brázdová A; Department of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
  • Drahota Z; Department of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
  • Houstek J; Department of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
  • Mrácek T; Department of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Biofactors ; 45(5): 703-711, 2019 Sep.
Article em En | MEDLINE | ID: mdl-31343786
ABSTRACT
Metformin is the most widely prescribed treatment of hyperglycemia and type II diabetes since 1970s. During the last 15 years, its popularity increased due to epidemiological evidence, that metformin administration reduces incidence of cancer. However, despite the ongoing effort of many researchers, the molecular mechanisms underlying antihyperglycemic or antineoplastic action of metformin remain elusive. Most frequently, metformin is associated with modulation of mitochondrial metabolism leading to lowering of blood glucose or activation of antitumorigenic pathways. Here we review the reported effects of metformin on mitochondrial metabolism and their potential relevance as effective molecular targets with beneficial therapeutic outcome.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Diabetes Mellitus Tipo 2 / Hiperglicemia / Hipoglicemiantes / Metformina / Mitocôndrias / Neoplasias / Antineoplásicos Idioma: En Ano de publicação: 2019 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Diabetes Mellitus Tipo 2 / Hiperglicemia / Hipoglicemiantes / Metformina / Mitocôndrias / Neoplasias / Antineoplásicos Idioma: En Ano de publicação: 2019 Tipo de documento: Article