Open AccessThe role of glucose metabolism and insulin resistance in cardiac remodelling induced by cigarette smoke exposure
Author(s) -
Azevedo Paula Schmidt,
Polegato Bertha F.,
Paiva Sergio,
Costa Nara,
Santos Priscila,
Bazan Silmeia,
Fernandes Ana Angelica Henrique,
Fabro Alexandre,
Pires Vanessa,
Tanni Suzana E.,
Leal Pereira Filipe,
Lo Angelo,
Grassi Leticia,
Campos Dijon,
Androcioli Vickeline,
Zornoff Leonardo,
Minicucci Marcos
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16053
Subject(s) - insulin resistance , cigarette smoke , carbohydrate metabolism , metabolism , medicine , endocrinology , insulin , environmental health
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.