Adiponectin (ApN) is considered to be responsible for reduction of inflammation and is known to be included in lipid metabolism. This study was designed to assess the role of adiponectin in patients with type 1 and type 2 diabetes and to determine parameters important in the prediction of adiponectin.Adiponectin, high sensitive C-reactive protein, fibrinogen, homocysteine, C-peptide, and lipid panel in addition to clinical and laboratory parameters important for the definition of diabetes, obesity and the metabolic syndrome were measured in 118 patients.The best model (R2=0.989) for predicting adiponectin in type 1 diabetes included fibrinogen, white blood cell count, uric acid and triglycerides. In type 2 diabetes the best model (R2=0.751) included C-peptide, white blood cell count, systolic blood pressure, fasting blood glucose, glycated hemoglobin and high-density lipoprotein cholesterol. ANOVA showed among-group differences in adiponectin (P=0.028), body mass index (P < 0.001), fasting blood glucose (P < 0.001) and high-density lipoprotein cholesterol (P =0.012) according to the type of diabetes. Between-group differences were also observed in adiponectin (P =0.033) and high-density lipoprotein cholesterol (P =0.009) according to sex. Adiponectin correlated (P < 0.05) with body mass index, C-peptide, pulse pressure and high-density lipoprotein cholesterol.Adiponectin levels were higher in type 1 diabetes. The association between C-peptide and adiponectin is probably one of the reasons for their different respective levels in different types of diabetes. Interrelations between adiponectin and inflammation, dyslipidemia, C-peptide levels and sex appear to be important for complex adiponectin modulation and action.
Aims: The study investigated the role of statin and ACE-inhibitor therapy in the development of atherosclerosis via their effect on C-reactive protein (CRP) and homocysteine (HCY). Methods: A total of 243 type 2 diabetics were studied during a 1-yr. follow-up period. Patients were randomized to receive either atorvastatin (n=59), simvastatin (n=64), pravastatin (n=38), or trandolapril (n=43). The control group included 39 patients. The patients were assigned to groups based on AER /mg/24h/ ( 300), pulse pressure (PP) ( 65) and body mass index (BMI) ( 30). Results: ANOVA revealed significant differences in initial CRP and atherogenic index of plasma (AIP) (p=0.01 and p=0.041, respectively) according to AER and BMI (both p<0.001), and in HCY and AIP (both p<0.001) according to PP. Multiple linear regression for CRP, HCY, age, diabetes duration, BMI, AIP, AER and PP showed (p<0.01) BMI and AIP to be independent predictors of CRP, and age, AER and BMI to be independent predictors of HCY (p<0.05). CRP was significantly reduced in the groups treated with atorvastatin (p<0.001), simvastatin (p=0.049) or trandolapril (p=0.012). HCY was significantly reduced in the simvastatin- and pravastatin-treated groups (p=0.015 vs. p=0.002) ; AIP and PP were significantly reduced in the simvastatin- and atorvastatin-treated groups (both p<0.01). A significant reduction (p<0.005) in AER and PP was revealed in the trandolapril group. Conclusions: ACE-inhibitors and statins had a beneficial effect on blood pressure and lipid profile, also attenuating inflammation by reducing CRP and HCY, and consequently delaying the development of atherosclerosis.
Adiponectin (ApN) is considered to be responsible for reduction of inflammation and is known to be included in lipid metabolism. This study was designed to assess the role of adiponectin in patients with type 1 and type 2 diabetes and to determine parameters important in the prediction of adiponectin. Adiponectin, high sensitive C-reactive protein, fibrinogen, homocysteine, C-peptide, and lipid panel in addition to clinical and laboratory parameters important for the definition of diabetes, obesity and the metabolic syndrome were measured in 118 patients included in the study. The best model (R2=0.989) for predicting adiponectin in type 1 diabetes included fibrinogen, white blood cell count, uric acid and triglycerides. In type 2 diabetes the best model (R2=0.751) included C-peptide, white blood cell count, systolic blood pressure, fasting blood glucose, glycated hemoglobin and high-density lipoprotein cholesterol. ANOVA showed statistically significant among-group differences in adiponectin (p=0.028), body mass index (p<0.001), fasting blood glucose (p<0.001) and high-density lipoprotein cholesterol (p=0.012) according to the type of diabetes. Significant between-group differences were also observed in adiponectin (p=0.033) and high-density lipoprotein cholesterol (p=0.009) according to sex. Adiponectin correlated significantly (p<0.05) with body mass index, C-peptide, pulse pressure and high-density lipoprotein cholesterol. Adiponectin levels were significantly higher in type 1 diabetes. The association between C-peptide and adiponectin is probably one of the reasons for their different respective levels in different types of diabetes. Interrelations between adiponectin and inflammation, dyslipidemia, C-peptide levels and sex appear to be important for complex adiponectin modulation and action.
Introduction: We studied potential benefits of statins and folic acid on lipids and markers of inflammation to investigate their role in the development of microangiopathy. Methods: A total of 259 type 2 diabetics were studied during a 1.5-yr. follow-up. Patients were randomised to receive either atorvastatin, pravastatin, simvastatin or folic acid. Homocysteine (HCY), C-reactive protein (CRP), lipid values, pulse pressure (PP), postprandial hyperglycaemia (PPG), aterogenic index of plasma (AIP) and albumin excretion rate (AER) were determined. The patients were assigned to groups based on AER /mg/24h/ ( 300), and PP ( 70). Results: ANOVA revealed significant differences in initial HCY, high density lipoprotein (HDL) and AIP (p<0.001 all) according to PP, and in initial CRP (p=0.041) according to AER. HDL was significantly increased in the simvastatin- and pravastatin-treated group (p=0.032 vs. p= 0.011). HCY was significantly reduced in simvastatin-, pravastatin- and folic acid-treated groups (p=0.012 vs. p=0.005 vs. p=0.001), primarily in patients with AER of 15-30 mg/24h (p=0.002). The reduction in HCY was most pronounced (Wilcoxon signed ranks test) in the folic acid-treated group (p<0.01). CRP was significantly reduced in the groups treated with atorvastatin (p<0.001) and simvastatin (p=0.008). AIP and PP were significantly reduced in simvastatin- and atorvastatin-treated groups (p<0.001 vs. p=0.002, and p<0.001 vs. p=0.009, respectively). Conclusion: Statin-induced increase in HDL and decrease in HCY, CRP, AIP and PP, as well as the folic acid-induced reduction in HCY could prevent or delay the onset of microangiopathy in diabetes.