This study investigated the role of sorbitol, a metabolic product of glucose, in the pathogenesis of rat diabetic cystopathy. Three-month-old male Wistar rats were divided into four groups: 1) normal controls; 2) rats rendered diabetic by streptozotocin; 3) rats fed with glucose; and 4) rats injected with sorbitol. The M2 muscarinic receptor (M2-mAChR) protein and mRNA densities of the bladder tissue were measured by Western immunoblot and Northern blot, respectively. The streptozotocin-induced diabetic rats were then treated with ONO-2235, an aldose reductase inhibitor. The bladder M2-mAChR protein and mRNA were compared between the treated and untreated diabetic rats. The densities of M2-mAChR protein and mRNA in the bladder tissue were significantly increased in diabetic rats, and rats given either glucose or sorbitol (increases in receptor protein: 27.3 ± 3.3, 19.8 ± 2.3, and 18.0 ± 2.1%; increases in mRNA: 39.6 ± 3.7, 33.1 ± 2.9, and 20.2 ± 2.2%, respectively). When diabetic rats were treated with ONO-2235, the increases in bladder M2mAChR protein and mRNA were significantly alleviated. The findings suggest that sorbitol plays a role in the pathogenesis of diabetic cystopathy in rats rendered diabetic by streptozotocin. Aldose reductase inhibitors may be useful in the treatment and prevention of diabetic cystopathy.
All Science Journal Classification (ASJC) codes
- Clinical Neurology