Article
Administration of granulocyte-colony stimulating factor accompanied with a balanced diet improves cardiac function alterations induced by high fat diet in mice.
Registro en:
DALTRO, P. S. et al. Administration of granulocyte-colony stimulating factor accompanied with a balanced diet improves cardiac function alterations induced by high fat diet in mice. BMC Cardiovascular Disorders, v. 15, p. 162, 2015.
1471-2261
10.1186/s12872-015-0154-6
Autor
Daltro, Pâmela Santana
Alves, Paula Santana
Castro, Murilo Fagundes de
Azevedo, Carine Machado
Vasconcelos, Juliana Fraga
Allahdadi, Kyan James
Freitas, Luiz Antonio Rodrigues de
Souza, Bruno Solano de Freitas
Santos, Ricardo Ribeiro dos
Soares, Milena Botelho Pereira
Macambira, Simone Garcia
Resumen
Background/Objectives: High fat diet (HFD) is a major contributor to the development of obesity and cardiovascular
diseases due to the induction of cardiac structural and hemodynamic abnormalities. We used a model of diabetic
cardiomyopathy in C57Bl/6 mice fed with a HFD to investigate the effects of granulocyte-colony stimulating
factor (G-CSF), a cytokine known for its beneficial effects in the heart, on cardiac anatomical and functional
abnormalities associated with obesity and type 2 diabetes.
Methods: Groups of C57Bl/6 mice were fed with standard diet (n = 8) or HFD (n = 16). After 36 weeks, HFD animals
were divided into a group treated with G-CSF + standard diet (n = 8) and a vehicle control group + standard diet
(n = 8). Cardiac structure and function were assessed by electrocardiography, echocardiography and treadmill tests, in
addition to the evaluation of body weight, fasting glicemia, insulin and glucose tolerance at different time points.
Histological analyses were performed in the heart tissue.
Results: HFD consumption induced metabolic alterations characteristic of type 2 diabetes and obesity, as well as cardiac
fibrosis and reduced exercise capacity. Upon returning to a standard diet, obese mice body weight returned to
non-obese levels. G-CSF administration accelerated the reduction in of body weight in obese mice. Additionally,
G-CSF treatment reduced insulin levels, diminished heart fibrosis, increased exercise capacity and reversed cardiac
alterations, including bradycardia, elevated QRS amplitude, augmented P amplitude, increased septal wall thickness, left
ventricular posterior thickening and cardiac output reduction.
Conclusion: Our results indicate that G-CSF administration caused beneficial effects on obesity-associated cardiac
impairment.