SUMMARYThis study was designed to determine whether the diabetic BioBreeding rat develops significant renal injury following long-term moderate to severe hyperglycaemia. Diabetic and control rats were followed from the onset of diabetes (2-4 months) to 18 months of age. Frank proteinuria and/or albuminuria were always absent. Glomerular filtration rate, measured by inulin clearance (ml min-' (100 g body weight)-1), was significantly higher in diabetic rats than in controls at 10, 12 and 18 months of age. Advanced glycosylation end-product cross-links assessed by percentage solubility of tail tendon collagen were moderately increased in diabetic compared with control animals. Urinary excretion of advanced glycosylation end-products in unfractionated urine and in urine fractionated for low molecular mass peptides (< 10 kDa) was 11-fold greater in the diabetic rats than in the control group. Urinary excretion of nitric oxide metabolites (nmol NO2 and NO3-(24 h)-1) were significantly (P < 0.05) greater in diabetic rats than in controls after 8 months of age. Mild histopathology resembling human diabetic nephropathy, including increased mesangial volume and glomerular basement membrane thickness, was detected at 18 months of age. The findings of hyperfiltration and mild glomerular morphological changes in diabetic BioBreeding rats are similar to the abnormalities seen in stage 2 human diabetic nephropathy. We hypothesize that two factors which may contribute to the resistance or tolerance to renal injury in the BioBreeding diabetic rat are increased nitric oxide production and the decreased accumulation of advanced glycosylation end-products.
Pentraxin 3 (PTX3) is an acute-phase protein that shares structural homology with C-reactive protein (CRP). Because obesity and metabolic syndrome (MetS) are considered chronic inflammatory states, PTX3 might be involved in the pathogenesis of obesity and MetS as well as CRP. In this study, we aimed to investigate the relationships between PTX3, CRP, body fat distribution and carotid intima media thickness (CIMT). 73 obese premenopousal women and 53 women with normal body mass index (BMI) took part in this study. Body fat distribution was evaluated by ulrasonography and by Bioelectrical Impedance Analysis (BIA). PTX3 was similar in both groups. PTX3 was also similar in obese patients with and without insulin resistance. CRP is significantly higher in obese patients (p < 0.01). It was also significantly higher in insulin resistance obese patients (p < 0.01). There was no correlation between BMI and any of the inflamatory markers. Multiple regression analysis showed that PTX3 is positively correlated with waist circumference (WC) (p = 0.036, beta = +0.436) and negatively correlated with subcutaneous fat (SCF) (p = 0.011, beta = -0.310). In conclusion, although PTX3 levels were not higher in obese patients and have no correlation with visceral fat, PTX3 levels were correlated with WC. In premenoposal obese women PTX3 levels were not related to subclinical atherosclerosis measured by CIMT.
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