title: Early cardiac changes induced by a hypercaloric Western-type diet in "subclinical" obesity.
abstract: "Obesity cardiomyopathy" effects have been widely described; however, the specific contribution of metabolic changes and altered adipokine secretion are still uncharacterized. Moreover, a diagnosis based on body mass index might not be the most accurate to identify increased adiposity and its outcomes. In this study, we aimed to determine the impact of a Western-type diet [hypercaloric diet (HCD)] ingestion on biventricular structure and function, as well as the metabolic and endocrine changes that occur before the establishment of overt obesity. Wistar rats were fed for 6 wk with a regular diet or HCD. At the end of the protocol, metabolic tests, cardiac structure, and functional evaluation were performed, and blood and tissue samples collected to perform histological, molecular biology, and functional studies. The animals that ingested the HCD presented increased adiposity and larger adipocyte cross-sectional area, but similar body weight compared with the regular diet group. At the cardiac level, HCD induced biventricular cardiomyocyte hypertrophy, fibrosis, increased stiffness, and impaired relaxation. Galectin-3 plasma expression was likewise elevated in the same animals. The nutritional modulation also altered the secretory pattern of the adipose tissue, originating a proinflammatory systemic environment. In this study, we observed that before "clinical" overweight or frank obesity is established, the ingestion of a HCD-induced cardiac remodeling manifests by increased biventricular stiffness and diastolic dysfunction. The mechanism triggering the cardiac alterations appears to be the proinflammatory environment promoted by the adipose tissue dysfunction. Furthermore, galectin-3, a profibrotic molecule, might be a potential biomarker for the myocardial alterations promoted by the HCD before overweight or obesity.
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal;
authors.forename: Nádia
authors.initials: N
authors.lastname: Gonçalves
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal;
authors.forename: Ana Filipa
authors.initials: AF
authors.lastname: Silva
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal;
authors.forename: Patrícia Gonçalves
authors.initials: PG
authors.lastname: Rodrigues
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal;
authors.forename: Eugénia
authors.initials: E
authors.lastname: Correia
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal; Department of Paediatric Cardiology, Centro Hospitalar São João, Porto, Portugal;
authors.forename: Cláudia
authors.initials: C
authors.lastname: Moura
authors.affiliation: Institute of Molecular Pathology and Immunology, Universidade do Porto, Porto, Portugal; and.
authors.forename: Catarina
authors.initials: C
authors.lastname: Eloy
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal;
authors.forename: Roberto
authors.initials: R
authors.lastname: Roncon-Albuquerque
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal; ipires@med.up.pt.
authors.forename: Inês
authors.identifier: http://orcid.org/0000-0003-1937-3782
authors.initials: I
authors.lastname: Falcão-Pires
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal; Department of Cardiothoracic Surgery, Centro Hospitalar São João, Porto, Portugal.
authors.forename: Adelino F
authors.initials: AF
authors.lastname: Leite-Moreira
mesh_terms: D017667:Adipocytes / Q000473:pathology*; D000273:Adipose Tissue; D000818:Animals; D001835:Body Weight; D009202:Cardiomyopathies / Q000000981:diagnostic imaging / Q000235:genetics / Q000473:pathology*; D048429:Cell Size; D024042:Collagen Type I / Q000235:genetics / Q000378:metabolism; D024061:Collagen Type III / Q000235:genetics / Q000378:metabolism; D003971:Diastole; D066273:Diet, Western; D004452:Echocardiography; D005109:Extracellular Matrix / Q000473:pathology; D005355:Fibrosis; D037502:Galectin 3 / Q000235:genetics* / Q000378:metabolism; D005951:Glucose Tolerance Test; D007249:Inflammation; D007333:Insulin Resistance; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000473:pathology*; D009765:Obesity; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D052243:Resistin / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology; D018754:Ventricular Dysfunction / Q000000981:diagnostic imaging / Q000235:genetics / Q000473:pathology*; D020257:Ventricular Remodeling
chemical_list: D024042:Collagen Type I; D024061:Collagen Type III; D037502:Galectin 3; C000594089:IL1B protein, rat; D053583:Interleukin-1beta; D020738:Leptin; D012333:RNA, Messenger; D052243:Resistin; C499622:Retn protein, rat; D014409:Tumor Necrosis Factor-alpha
keywords: adipose tissue; heart; hypercaloric diet; inflammation; remodeling