Autor(es):
Azevedo, Paula Schmidt [UNESP] ; Polegato, Bertha F. [UNESP] ; Paiva, Sergio [UNESP] ; Costa, Nara ; Santos, Priscila [UNESP] ; Bazan, Silmeia [UNESP] ; Fernandes, Ana Angelica Henrique [UNESP] ; Fabro, Alexandre ; Pires, Vanessa [UNESP] ; Tanni, Suzana E. [UNESP] ; Leal Pereira, Filipe [UNESP] ; Lo, Angelo [UNESP] ; Grassi, Leticia [UNESP] ; Campos, Dijon ; Androcioli, Vickeline [UNESP] ; Zornoff, Leonardo [UNESP] ; Minicucci, Marcos [UNESP]
Data: 2021
Identificador Persistente: http://hdl.handle.net/11449/206940
Origem: Oasisbr
Assunto(s): cardiac remodelling; cigarette smoke; glucose metabolism; heart failure; ventricular remodelling
Descrição
Made available in DSpace on 2021-06-25T10:46:23Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-01-01
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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.
Department of Internal Medicine Botucatu Medical School São Paulo State University-UNESP
Faculty of Nutrition UFG – Univ Federal de Goiás
Department of Chemical and Biological Sciences São Paulo State University-UNESP
Department of Pathology and Legal Medicine Ribeirão Preto Medical School University of São Paulo
Experimental Research Unit – UNIPEX Botucatu Medical School São Paulo State University-UNESP
Department of Internal Medicine Botucatu Medical School São Paulo State University-UNESP
Department of Chemical and Biological Sciences São Paulo State University-UNESP
Experimental Research Unit – UNIPEX Botucatu Medical School São Paulo State University-UNESP
CAPES: 001
FAPESP: 2014/24197-0
FAPESP: 2016/14547-0
FAPESP: 2016/25676-5
