Cardiac dysfunction in sucrose-fed rats is associated with alterations of phospholamban phosphorylation and TNF-α levels

• Published in: Molecular and cellular endocrinology Vol. 589; p. 112236
• Main Authors: Gregolin, Cristina Schmitt, do Nascimento, Milena, de Souza, Sérgio Luiz Borges, Mota, Gustavo Augusto Ferreira, Luvizotto, Renata de Azevedo Melo, Sugizaki, Mário Mateus, Bazan, Silméia Garcia Zanati, de Campos, Dijon Henrique Salomé, Camacho, Camila Renata Corrêa, Cicogna, Antonio Carlos, do Nascimento, André Ferreira
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 01.08.2024
• Subjects: Animals; Calcium handling; Calcium-Binding Proteins - metabolism; Cardiac function; Diet-induced obesity; Interleukin-6 - metabolism; Male; Myocardial Contraction - drug effects; Myocardium - metabolism; Myocardium - pathology; Phosphorylation - drug effects; Rats; Rats, Wistar; Sucrose; Sucrose - adverse effects; Tumor Necrosis Factor-alpha - metabolism; Diet-induced obesity; Calcium handling; Sucrose; Cardiac function
• ISSN: 0303-7207; 1872-8057; 1872-8057
• DOI: 10.1016/j.mce.2024.112236

High sucrose intake is linked to cardiovascular disease, a major global cause of mortality worldwide. Calcium mishandling and inflammation play crucial roles in cardiac disease pathophysiology. Evaluate if sucrose-induced obesity is related to deterioration of myocardial function due to alterations in the calcium-handling proteins in association with proinflammatory cytokines. Wistar rats were divided into control and sucrose groups. Over eight weeks, Sucrose group received 30% sucrose water. Cardiac function was determined in vivo using echocardiography and in vitro using papillary muscle assay. Western blotting was used to detect calcium handling protein; ELISA assay was used to assess TNF-α and IL-6 levels. Sucrose led to cardiac dysfunction. RYR2, SERCA2, NCX, pPBL Ser16 and L-type calcium channels were unchanged. However, pPBL-Thr17, and TNF-α levels were elevated in the S group. Sucrose induced cardiac dysfunction and decreased myocardial contractility in association with altered pPBL-Thr17 and elevated cardiac pro-inflammatory TNF-α. [Display omitted] •Sucrose consumption is able to induce in vivo and in vitro cardiac dysfunction.•Sucrose-induced cardiac dysfunction linked to intrinsic myocardial abnormalities.•Ca2+ mishandling is a potential mechanism in sucrose-induced cardiac dysfunction.•Inflammation may link sucrose-induced heart dysfunction and Ca2+ mishandling.