Abstract
Background and objectives: The aim of our study was to evaluate the role of diabetes mellitus (DM) as a significant factor affecting spontaneous stone expulsion, as suggested by previous research. Materials and methods: We investigated the influence of DM on the ureter using a murine model. The mouse-model arm of this study used 20 15 -week-old mice, including 10 normal (control) mice and 10 DM mice. We measured the proximal, middle and distal ureteral smooth muscle thickness in each mouse and the differences among ureteral sections were analyzed. Mouse ureteral specimens were also analyzed via western blotting to detect relative protein expression of phosphor–extracellular signal regulated kinases (P–ERK), phosphor–C–Jun N–terminal kinase (P–JNK), vascular endothelial growth factor (VEGF), and protein kinase C (PKC), which are representative factors involved in cell regulation. Results: We observed significant hyperproliferation of ureteral smooth muscle in DM mice compared to normal mice, which may provoke reduced peristalsis. The ureteral smooth muscle of DM mice was significantly thicker than that of normal mice in all ureteral tissues: proximal (p = 0.040), mid (p = 0.010), and distal (p = 0.028). The relative protein expression of P-ERK (p = 0.005) and P–JNK (p = 0.001) was higher in the diabetic group compared to the normal group. Additionally, protein expression of VEGF (p = 0.002) and PKC (p = 0.001) were remarkably up-regulated in DM mice. Conclusions: Hyperproliferation of ureteral smooth muscle was observed in DM mice, but not in normal mice. The pathways mediated by P–ERK, P–JNK, VEGF, and PKC may play an important role in pathological ureteral conditions.
Highlights
Introduction published maps and institutional affilDiabetes mellitus (DM) is a carbohydrate metabolism disorder caused by various etiological factors and generally involves absolute or relative insulin insufficiency, or insulin resistance, resulting in blood glucose elevation
As part of compensatory changes for impaired contractility, increased cellular proliferation was observed in patients with diabetes-associated cystopathy
Underlying diabetes mellitus (DM) affects the thickening of the ureter and is known to be a cause of adverse effects on the spontaneous passage of ureteral stones
Summary
Diabetes mellitus (DM) is a carbohydrate metabolism disorder caused by various etiological factors and generally involves absolute or relative insulin insufficiency, or insulin resistance, resulting in blood glucose elevation. DM is strongly associated with various types of genitourinary system infections, such as pyelonephritis and Fournier’s gangrene, and increases the chances of stone formation, especially those made of uric acid. A recent study of 574 patients demonstrated that DM was independently associated with the presence of stones [1]. As part of compensatory changes for impaired contractility, increased cellular proliferation was observed in patients with diabetes-associated cystopathy. The aim of our study was to evaluate the role of diabetes mellitus (DM) as a significant factor affecting spontaneous stone expulsion, as suggested by previous research
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