RESUMEN
BACKGROUND: Obesity is a global problem associated with several conditions, including hypertension, diabetes, arthritis and cardiovascular diseases. With the increase in the prevalence of obesity in recent years, mostly in developing countries, it is important to study its impact on various diseases, including infectious illnesses, such as Chagas disease, caused by the protozoan Trypanosoma cruzi. Considering that a diet rich in salt, sugar, and fat is associated with obesity, this study aimed to evaluate the influence of cafeteria diet (CAF)-induced obesity on immune responses in T. cruzi-infected rats. METHODS: Male Wistar Hannover rats were provided with water and food ad libitum (chow group). The CAF-fed groups received a normal rodent diet or CAF. The animals were intraperitoneally infected with 105 trypomastigote forms of the Y strain of T. cruzi present in the whole blood from a previously infected mouse. RESULTS: CAF-fed rats showed a significant increase in visceral adipose tissue weight compared to chow-fed rats. A significant reduction in CD3+ CD4+ helper splenic T cells was observed in obese-infected rats compared to non-obese-infected rats, as well as CD11b and macrophages. In addition, macrophages from obese animals displayed reduced RT1b levels compared to those from control animals. Moreover, INF-γ, an important factor in macrophage activation, was reduced in obese-infected rats compared with their counterparts. CONCLUSIONS: These results indicate that a CAF can impair the cell-mediated immune response against T. cruzi.
Asunto(s)
Enfermedad de Chagas , Trypanosoma cruzi , Ratas , Masculino , Ratones , Animales , Ratas Wistar , Obesidad , Dieta , InmunidadRESUMEN
Subclinical hyperthyroidism (SH) may be responsible for many cardiovascular changes, including an impaired exercise performance. The aim of our study was to evaluate the response to the treadmill cardiopulmonary test in patients with SH. We studied 14 female patients from our endocrine clinic with exogenous SH, free from cardiovascular diseases, with mean age of 38.6 +/- 10.2 years, body mass index (BMI) of 24.4 +/- 4.0 kg/m(2), and disease duration of 4.9 +/- 4.9 years. The mean serum thyrotropin (TSH) was 0.03 +/- 0.03 mU/L, serum free thyroxine (FT(4)), 1.72 +/- 0.21 ng/dL, and serum triiodothyronine level, 137 +/- 32 ng/dL. The control group comprised 15 euthyroid, healthy women, with mean age of 35.4 +/- 7.4 years and BMI of 27.3 +/- 5.9 kg/m(2). Both groups had a sedentary lifestyle and underwent the cardiopulmonary test using a treadmill with the Balke protocol. Gas concentrations and the respiratory outflow were measured and the electrocardiogram (ECG) was registered in real time. We calculated the minute ventilation (V(E)), the oxygen consumption (peak VO(2)), the carbonic gas exhalation (peak VCO(2)) and the anaerobic threshold (AT). The heart rate (HR) at rest (90.9 +/- 15.7 versus 78.9 +/- 8.7 beats per minute; p = 0.03) was higher in the patients from our clinic. There was no difference between groups regarding age, BMI, fat percentage, blood pressure, peak HR, exercise duration, mean treadmill peak inclination, V(E), peak VO(2), peak VCO(2), and AT. There was no correlation between peak VO(2) and FT(4), TSH, or disease duration. Our results show that exercise capacity in young and middle-aged female patients is not significantly affected by exogenous SH.