Metabolic profile of patients with endometrial adenocarcinoma and association with tumor grade.

OBJECTIVE: To describe the prevalence of metabolic syndrome and other metabolic indicators in patients with endometrial cancer and its association with tumor grade. METHODS: This is a cross-sectional study of patients with endometrial cancer referred to the Brazilian National Cancer Institute. We collected data on sociodemographic variables, smoking, co-morbidities, physical activity level, menopausal status, and tumor characteristics (histological subtype, stage, and tumor grade). In addition, weight, height, and waist circumference were measured. Laboratory evaluation included lipid profile, fasting blood glucose and insulin, and C-reactive protein. Insulin resistance was estimated by the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Characterization of metabolic syndrome and cardiovascular risk profile was performed. Binary logistic regression models were used to test the association between metabolic syndrome and its metabolic parameters, HOMA-IR, and C-reactive protein with tumor grade. RESULTS: We included a total of 313 patients, 245 (78.3%) aged <65 years, 262 (83.7%) with endometrioid adenocarcinoma, 193 (61.7%) early stage, and 201 (64.2%) with lower tumor grade (G1 and G2). Metabolic syndrome, insulin resistance, and low levels of leisure-time physical activity were highly prevalent (90.7%). In binary logistic regression models, an association was observed between HOMA-IR and lower tumor grade (p<0.05), while high-grade tumors were associated with the highest C-reactive protein values (p<0.05). CONCLUSION: The main finding of this study was the association between insulin resistance and low-grade tumors, and the association between high C-reactive protein levels and high-grade tumors.

Resistance exercise prevents impaired homocysteine metabolism and hepatic redox capacity in Walker-256 tumor-bearing male Wistar rats.

OBJECTIVE: The aim of this study was to investigate changes in homocysteine (Hcy) metabolism and redox balance in response to exercise treatment in a tumor-bearing rat model. METHODS: Male Wistar rats were exposed, or not, to a resistance exercise program 6 wk before inoculation with Walker-256 tumor cells or vehicle. After application, rats maintained their routine for 12 d and were then sacrificed for plasma and liver analyses. RESULTS: Impaired Hcy metabolism was evident after 12 d of tumor cell inoculation as demonstrated by significantly increased (P < 0.05) plasma total homocysteine (tHcy) concentration (53%) and decreased plasma cysteine, methionine, and vitamin B12 concentrations. Decreased hepatic cystathionine ß-synthase (CBS) and betaine-homocysteine S-methyltransferase mRNA levels were found in tumor-bearing rats but not in controls. Tumor inoculation also decreased levels of liver reduced glutathione (GSH) and increased hepatic oxidative stress compared with non-tumor controls. However, resistance exercise prevented the tumor-impaired transsulfuration pathway as demonstrated by the decreased plasma tHcy, hepatic CBS expression, and increased GSH in tumor-exercised versus tumor-sedentary rats. Remarkably, all measures of liver oxidative stress were suppressed by exercise training. Tumor weight was unchanged between groups. CONCLUSION: Resistance exercise prevented tHcy accumulation and liver oxidative damage caused by Walker-256 tumor cell inoculation; the modulatory effects of resistance exercise on Hcy metabolism appear to be at the level of transsulfuration pathway.