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      Glomerular Cell Replication and Cell Loss through Apoptosis in Experimental Diabetes mellitus

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          Aim: To evaluate changes in the glomerular cell balance between replication and apoptosis in experimental diabetes mellitus (DM) in relation to morphometric data. Methods: Adult Sprague-Dowley rats with streptozotocin-induced DM and controls of the same age and strain were sacrificed 4 and 8 weeks and 6 months after disease onset. Cell replication was demonstrated with MIB-5, and apoptosis with the terminal uridine nick end labeling technique. Glomerular size and glomerular cell population were estimated morphologically. Results: Diabetic and control rats showed irrelevant MIB-5 positivity at all time points. Glomerular apoptosis was minimal in rats with 4 and 8 weeks of DM and in controls. Rats with 6 months of DM showed significantly higher glomerular apoptosis values than controls (2.49 ± 0.25 vs. 0.65 ± 0.16%; p < 0.001). The mean cell count per glomerular profile was significantly lower in these diabetic rats (64.02 ± 1.93 vs. 78.27 ± 0.99; p < 0.001), a change that correlated with that in apoptosis. The glomerular cell density was further decreased in diabetic rats because of the diabetic increase in mean glomerular volume (1.598 vs. 0.927 10<sup>6</sup> µm). Conclusions: Apoptosis is associated with loss of glomerular cells in rats with long-term, streptozotocin-induced DM and – to a considerably lower degree – in controls of the same age and strain. These changes could be relevant to glomerulosclerosis associated with long-term, streptozotocin-induced DM.

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          Glucose loading induces DNA fragmentation in rat proximal tubular cells.

           K Numakami,  H Itoh,  T Saruta (1996)
          A 10% glucose, 10% mannitol, or 0.9% saline solution was infused in male Wistar rats for 300 minutes via the left cervical vein. Glomerular filtration rates (GFRs) were not significantly altered in any of the three groups. DNA was extracted from isolated proximal tubular cells at the end of each infusion. Electrophoresis on agarose gels showed a distinct ladder pattern of DNA fragmentation in 10% glucose-loaded rats, but no such pattern in 10% mannitol- or 0.9% saline-loaded rats. After infusion for 300 minutes, the plasma glucose level of the 10% glucose-loaded group was higher than that of the other two groups (each P < .005). These results suggest that hyperglycemia led to DNA fragmentation in the DNA of proximal tubular cells, similar to the process of programmed cell death known as apoptosis. DNA fragmentation may be associated with renal proximal tubular damage in the early stages of diabetic nephropathy.

            Author and article information

            S. Karger AG
            April 2002
            08 April 2002
            : 90
            : 4
            : 484-488
            aCentro di Anatomia Patologica, DISTBIMO, Università di Genova, bLaboratorio di Metabolismo e Biochimica Patologica, Istituto Superiore di Sanità, Roma, e cCattedra di Endocrinologia, Dipartimento di Science Cliniche, Università La Sapienza, Roma, Italia
            54738 Nephron 2002;90:484–488
            © 2002 S. Karger AG, Basel

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            Page count
            Figures: 2, References: 24, Pages: 5
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            Original Paper

            Cardiovascular Medicine, Nephrology

            Diabetes mellitus, Cell replication, Glomerulosclerosis, Apoptosis


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