Adipocytokines and breast cancer risk / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Many researches suggested that obesity increased the risk of breast cancer, but the mechanism was currently unknown. Adipocytokines might mediate the relationship. Our study was aimed to investigate the relationship between serum levels of resistin, adiponectin and leptin and the onset, invasion and metastasis of breast cancer.</p><p><b>METHODS</b>Blood samples were collected from 80 newly diagnosed, histologically confirmed breast cancer patients and 50 age-matched healthy controls. Serum levels of resistin, adiponectin and leptin were determined by enzyme-linked immunosorbent assays (ELISA); fasting blood glucose (FBG), lipids, body mass index (BMI), and waist circumference (WC) were assayed simultaneously.</p><p><b>RESULTS</b>Serum levels of adiponectin ((8.60 +/- 2.92) mg/L vs (10.37 +/- 2.81) mg/L, P = 0.001) and HDL-c were significantly decreased in breast cancer patients in comparison to controls. Serum levels of resistin ((26.35 +/- 5.36) microg/L vs (23.32 +/- 4.75) microg/L, P = 0.000), leptin ((1.35 +/- 0.42) microg/L vs (1.06 +/- 0.39) microg/L, P = 0.003), FBG and triglyceride (TG) in breast cancer patients were increased in contrast to controls, respectively. However, we did not find the significant difference of the serum levels of resistin, adiponectin and leptin between premenopausal breast cancer patients and healthy controls (P = 0.091, 0.109 and 0.084, respectively). The serum levels of resistin, adiponectin and leptin were significantly different between patients with lymph node metastasis (LNM) and those without LNM (P = 0.001, 0.000 and 0.006, respectively). The stepwise regression analysis indicated that the tumor size had the close correlation with leptin (R(2) = 0.414, P = 0.000) and FBG (R(2) = 0.602, P = 0.000). Logistic regression analysis showed that reduced serum levels of adiponectin (OR: 0.805; 95% CI: 0.704 - 0.921; P = 0.001), HDL (OR: 0.087; 95% CI: 0.011 - 0.691, P = 0.021), elevated leptin (OR: 2.235; 95% CI: 1.898 - 4.526; P = 0.004) and resistin (OR: 1.335; 95% CI: 1.114 - 2.354; P = 0.012) increased the risk for breast cancer; Reduced serum levels of adiponectin (OR: 0.742; 95% CI: 0.504 - 0.921; P = 0.003) and elevated leptin (OR: 2.134; 95% CI: 1.725 - 3.921; P = 0.001) were associated with lymph node metastasis of breast cancer.</p><p><b>CONCLUSIONS</b>The decreased serum adiponectin levels and increased serum resistin and leptin levels are risk factors of breast cancer. The low serum adiponectin levels and high serum leptin levels are independent risk factors for metastasis of cancer. The association between obesity and breast cancer risk might be explained by adipocytokines.</p>

Influence of blood glucose on the expression of glucose trans-porter proteins 1 and 3 in the brain of diabetic rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The delivery of glucose from the blood to the brain involves its passage across the endothelial cells of the blood-brain barrier (BBB), which is mediated by the facilitative glucose transporter protein 1 (GLUT(1)), and then across the neural cell membranes, which is mediated by GLUT(3). This study aimed to evaluate the dynamic influence of hyperglycemia on the expression of these GLUTs by measuring their expression in the brain at different blood glucose levels in a rat model of diabetes. This might help to determine the proper blood glucose threshold level in the treatment of diabetic apoplexy.</p><p><b>METHODS</b>Diabetes mellitus was induced with streptozotocin (STZ) in 30 rats. The rats were randomly divided into 3 groups: diabetic group without blood glucose control (group DM1), diabetic rats treated with low dose insulin (group DM2), and diabetic rats treated with high dose insulin (group DM3). The mRNA and protein levels of GLUT(1) and GLUT(3) were assayed by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry, respectively.</p><p><b>RESULTS</b>Compared with normal control rats, the GLUT(1) mRNA was reduced by 46.08%, 29.80%, 19.22% (P < 0.01) in DM1, DM2, and DM3 group, respectively; and the GLUT(3) mRNA was reduced by 75.00%, 46.75%, and 17.89% (P < 0.01) in DM1, DM2, and DM3 group, respectively. The abundance of GLUT(1) and GLUT(3) proteins had negative correlation with the blood glucose level (P < 0.01). The density of microvessels in the brain of diabetic rats did not change significantly compared with normal rats.</p><p><b>CONCLUSIONS</b>Chronic hyperglycemia downregulates GLUT(1) and GLUT(3) expression at both mRNA and protein levels in the rat brain, which is not due to the decrease of the density of microvessels. The downregulation of GLUT(1) and GLUT(3) expression might be the adaptive reaction of the body to prevent excessive glucose entering the cell that may lead to cell damage.</p>