Abstract:
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.
journal_name
BMC Cardiovasc Disordjournal_title
BMC cardiovascular disordersauthors
Daltro PS,Alves PS,Castro MF,Azevedo CM,Vasconcelos JF,Allahdadi KJ,de Freitas LA,de Freitas Souza BS,Dos Santos RR,Soares MB,Macambira SGdoi
10.1186/s12872-015-0154-6subject
Has Abstractpub_date
2015-12-03 00:00:00pages
162issn
1471-2261pii
10.1186/s12872-015-0154-6journal_volume
15pub_type
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