The role of glucose metabolism and insulin resistance in cardiac remodelling induced by cigarette smoke exposure.
cardiac remodelling
cigarette smoke
glucose metabolism
heart failure
ventricular remodelling
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
20
08
2020
revised:
08
10
2020
accepted:
11
10
2020
pubmed:
11
12
2020
medline:
15
9
2021
entrez:
10
12
2020
Statut:
ppublish
Résumé
The aim of this study is to evaluate whether the alterations in glucose metabolism and insulin resistance are mechanisms presented in cardiac remodelling induced by the toxicity of cigarette smoke. Male Wistar rats were assigned to the control group (C; n = 12) and the cigarette smoke-exposed group (exposed to cigarette smoke over 2 months) (CS; n = 12). Transthoracic echocardiography, blood pressure assessment, serum biochemical analyses for catecholamines and cotinine, energy metabolism enzymes activities assay; HOMA index (homeostatic model assessment); immunohistochemistry; and Western blot for proteins involved in energy metabolism were performed. The CS group presented concentric hypertrophy, systolic and diastolic dysfunction, and higher oxidative stress. It was observed changes in energy metabolism, characterized by a higher HOMA index, lower concentration of GLUT4 (glucose transporter 4) and lower 3-hydroxyl-CoA dehydrogenase activity, suggesting the presence of insulin resistance. Yet, the cardiac glycogen was depleted, phosphofructokinase (PFK) and lactate dehydrogenase (LDH) increased, with normal pyruvate dehydrogenase (PDH) activity. The activity of citrate synthase, mitochondrial complexes and ATP synthase (adenosine triphosphate synthase) decreased and the expression of Sirtuin 1 (SIRT1) increased. In conclusion, exposure to cigarette smoke induces cardiac remodelling and dysfunction. The mitochondrial dysfunction and heart damage induced by cigarette smoke exposure are associated with insulin resistance and glucose metabolism changes.
Identifiants
pubmed: 33300293
doi: 10.1111/jcmm.16053
pmc: PMC7812248
doi:
Substances chimiques
Catecholamines
0
Glucose
IY9XDZ35W2
Cotinine
K5161X06LL
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1314-1318Subventions
Organisme : Fundação de Amparo à Pesquisa do Estado de São Paulo
ID : 2014/24197-0
Organisme : Fundação de Amparo à Pesquisa do Estado de São Paulo
ID : 2016/25676-5
Organisme : Fundação de Amparo à Pesquisa do Estado de São Paulo
ID : 2016/14547-0
Organisme : Conselho Nacional de Pesquisa, Ministério da Ciência, Tecnologia, Inovações e Comunicações
Organisme : Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
ID : 001
Informations de copyright
© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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