The role of glucose metabolism and insulin resistance in cardiac remodelling induced by cigarette smoke exposure

Autor(es):Mostrar menos -

Azevedo, Paula Schmidt ^[1] ; Polegato, Bertha F. ^[1] ; Paiva, Sergio ^[1] ; Costa, Nara ^[2] ; Santos, Priscila ^[1] ; Bazan, Silmeia ^[1] ; Henrique Fernandes, Ana Angelica ^[3] ; Fabro, Alexandre ^[4] ; Pires, Vanessa ^[1] ; Tanni, Suzana E. ^[1] ; Pereira, Filipe Leal ^[1] ; Lo, Angelo ^[1] ; Grassi, Leticia ^[1] ; Campos, Dijon ^[4] ; Androcioli, Vickeline ^[5] ; Zornoff, Leonardo ^[1] ; Minicucci, Marcos ^[1]

Afiliação do(s) autor(es)

^[1] Sao Paulo State Univ UNESP, Botucatu Med Sch, Dept Internal Med, Av Prof Mario Rubens Guimaraes Montenegro S-N, BR-18618687 Botucatu, SP - Brazil

^[2] UFG Univ Fed Goias, Fac Nutr, Goiania, Go - Brazil

^[3] Sao Paulo State Univ UNESP, Dept Chem & Biol Sci, Botucatu, SP - Brazil

^[4] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pathol & Legal Med, Ribeirao Preto - Brazil

^[5] Sao Paulo State Univ UNESP, Botucatu Med Sch, Expt Res Unit UNIPEX, Botucatu, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF CELLULAR AND MOLECULAR MEDICINE; v. 25, n. 2 DEC 2020.
• Citações Web of Science: 0

Resumo

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. (AU)

• Processo FAPESP: 14/24197-0 - O papel do metabolismo da glicose na cardiomiopatia induzida pela exposição à fumaça de cigarros
• Beneficiário: Paula Schmidt Azevedo Gaiolla
• Linha de fomento: Auxílio à Pesquisa - Regular
• Processo FAPESP: 16/14547-0 - Influência da metformina no metabolismo energético cardíaco de ratos expostos á fumaça de cigarros
• Beneficiário: Vanessa de Cássia Martins Pires Ferreira
• Linha de fomento: Bolsas no Brasil - Mestrado
• Processo FAPESP: 16/25676-5 - Influência da metformina no remodelamento cardíaco de ratos expostos à fumaça de cigarros
• Beneficiário: Letícia Dalla Vecchia Grassi
• Linha de fomento: Bolsas no Brasil - Iniciação Científica