| Full text | |
| Author(s): Show less - |
Pedro Henrique Rizzi Alves
[1]
;
Artur Junio Togneri Ferron
[2]
;
Mariane Róvero Costa
[3]
;
Fabiana Kurokawa Hasimoto
[4]
;
Cristina Schmitt Gregolin
;
Jéssica Leite Garcia
[6]
;
Dijon Henrique Salomé de Campos
[7]
;
Antônio Carlos Cicogna
[8]
;
Letícia de Mattei
[9]
;
Fernando Moreto
[10]
;
Silméia Garcia Zanati Bazan
[11]
;
Fabiane Valentini Francisqueti-Ferron
[12]
;
Camila Renata Corrêa
[13]
Total Authors: 13
|
| Affiliation: Show less - | [1] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[2] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[3] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[4] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[6] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[7] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[8] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[9] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[10] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[11] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[12] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
[13] Universidade Estadual Paulista Júlio de Mesquita Filho. Faculdade de Medicina - Brasil
Total Affiliations: 13
|
| Document type: | Journal article |
| Source: | Arquivos Brasileiros de Cardiologia; v. 117, n. 1, p. 91-99, 2021-07-26. |
| Abstract | |
Abstract Background Obesity is a chronic low-grade inflammation condition related to cardiac disorders. However, the mechanism responsible for obesity-related cardiac inflammation is unclear. The toll-like receptor 4 (TLR-4) belongs to a receptor of the transmembrane family responsible for the immune response whose activation stimulates the production of proinflammatory cytokines. Objective To test whether the activation of the TLR-4 receptor participates in the obesity cardiomyopathy process, due to cytokine production through NF-ĸB activation. Methods Male Wistar rats were randomized into two groups: the control group (C, n= 8 animals) that received standard diet/water and the obese group (OB, n= 8 animals) that were fed a high sugar-fat diet and water plus 25% of sucrose for 30 weeks. Nutritional analysis: body weight, adiposity index, food, water, and caloric intake. Obesity-related disorders analysis: plasma glucose, uric acid and triglycerides, HOMA-IR, systolic blood pressure, TNF-α in adipose tissue. Cardiac analysis included: TLR-4 and NF-ĸB protein expression, TNF-α and IL-6 levels. Comparison by unpaired Student’s t-test or Mann- Whitney test with a p-value < 0.05 as statistically significant. Results The OB group showed obesity, high glucose, triglycerides, uric acid, HOMA, systolic blood pressure, and TNF-α in adipose tissue. OB group presented cardiac remodeling and diastolic dysfunction. TLR-4 and NF-ĸB expression and cytokine levels were higher in OB. Conclusion Our findings conclude that, in an obesogenic condition, the inflammation derived from cardiac TLR-4 activation can be a mechanism able to lead to remodeling and cardiac dysfunction. (AU) | |
| FAPESP's process: | 16/13592-1 - ANALYSIS OF GENE EXPRESSION OF TLR4 and TNF-± IN OBESE RATS MYOCARDIAL |
| Grantee: | Pedro Henrique Rizzi Alves |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |
| FAPESP's process: | 15/10626-0 - Interrelation of gamma-oryzanol and activation of adipose R1 and R2 adipose receptors: possible effect on improvement of obesity-associated renal function |
| Grantee: | Camila Renata Corrêa |
| Support Opportunities: | Regular Research Grants |