Effects of sympatholytic therapy with moxonidine on serum adiponectin levels in hypertensive women.

We examined whether moxonidine influences lipid profile, insulin resistance, adiponectin levels, renal function and microalbuminuria in women with essential hypertension in a study of 55 non-diabetic hypertensive patients and 53 normotensive women. Hypertensive patients received moxonidine for 12 weeks. At baseline the hypertensive group had significantly higher mean blood pressure, low-density lipoprotein cholesterol, triglycerides, total cholesterol, fasting glucose, urinary albumin excretion and homeostasis model assessment of insulin resistance (HOMA-IR), together with significantly lower mean high-density lipoprotein cholesterol, creatinine clearance and serum adiponectin than the normotensive group. Moxonidine significantly decreased blood pressure, fasting glucose, triglycerides, total cholesterol, HOMA-IR and albumin excretion, but significantly increased serum adiponectin. The change in adiponectin level was negatively correlated with the change in HOMA-IR. Moxonidine treatment may improve unfavourable metabolic status related to insulin resistance by increasing adiponectin levels in patients with essential hypertension. Since it can improve adiponectin levels, it may be used in the antihypertensive treatment of patients at high risk of diabetes and cardiovascular disease.

Adiponectin and insulin resistance in obesity-related diseases.

The relationship between insulin resistance and serum adiponectin levels in 400 subjects with different obesity-related diseases was studied. Lean subjects with body mass index (BMI) < 25 kg/m(2) were placed in one group and the other five groups of overweight/obese subjects with BMI >or= 25 kg/m(2) were grouped according to disease profile. The homeostasis model assessment insulin resistance (HOMA-IR) index and adiponectin levels were similar in the lean, metabolically normal (MNO) and hypertensive groups, but were different when the dyslipidaemic group was compared with the lean and MNO groups. The type 2 diabetic (DMO) and hypertensive, type 2 diabetic (DMHTO) groups were significantly different from other groups with respect to HOMA-IR index and adiponectin levels. Adiponectin levels were lower in the DMHTO than the DMO group. In multiple regression analysis, adiponectin levels correlated with group categorization independently of age, sex, BMI and HOMA-IR. Hypoadiponectinaemia may play a role in the development of complications of obesity.

Vascular endothelial growth factor, c-erbB-2 and c-erbB-3 expression in colorectal adenoma and adenocarcinoma.

AIM: To analyze vascular endothelial growth factor (VEGF), c-erbB-2 and c-erbB-3 expression and to evaluate their relation to clinicopathologic parameters and pathogenesis of colorectal carcinoma. METHODS: Sections of adenoma, intramucosal carcinoma and adenocarcinoma were evaluated by immunohistochemistry in 85 malignant and 37 benign colorectal neoplasms for the expression of VEGF, c-erbB-2 and c-erbB-3 considering clinicopathological variables. RESULTS: VEGF was detected in comparable percentages of all neoplasm types while c-erbB-2 expression was detectable more frequently in adenoma than adenocarcinoma cases (65% vs 43%). Except for the correlation of c-erbB-3 expression with Dukes' staging, there was no correlation between the studied markers and grade of differentiation, Dukes' stage and localization of colorectal adenocarcinoma. c-erbB-3 expression was seen more frequently in tubular adenomas, while c-erbB-2 expression was higher in tubulovillous and villous types. These differences were not statistically significant. The presence of distant metastasis and angiolymphatic invasion were identified as independent predictors of survival. A positive correlation was found between VEGF expression and lymphatic vessel invasion and regional lymph node involvement. CONCLUSION: These results suggest that VEGF, c-erbB-2, c-erbB-3 expression does not have prognostic value in colorectal cancer. VEGF expression may be implicated in the lymph node metastasis.