Role for the urinary bladder in pathogenesis of metabolic syndrome in Wistar rats

Perfusion of rat urinary bladder with uric acid (UA) or 1-methyl uric acid (1-MUA) solution was reported to produce features of metabolic syndrome, viz. hyperglycaemia, hyperinsulinaemia, hypertriglyceridaemia and hypercholesterolaemia. The present study was carried out to confirm that UA or 1-MUA in the bladder can produce insulin resistance, and to demonstrate that an unknown humoral factor from the bladder is possibly involved in producing features of metabolic syndrome.

Wistar rats weighing 200-300 g were used. Two sets of protocols, perfusion study and cross-over study, were followed. For the perfusion study, urinary bladders were perfused with distilled water or solution of UA or 1-MUA, and serum levels of glucose and insulin and insulin resistance during perfusion were compared between groups. For the cross-over study, serum from distilled water or UA perfused rats (donors) was infused intravenously into rats (recipients), and serum levels of glucose, insulin, true triglyceride and total cholesterol and insulin resistance were compared.

Perfusion of bladder with UA or 1-MUA solution resulted in an increase in serum levels of glucose and insulin, and insulin resistance, on comparison with distilled water perfused. Infusion of serum from donors perfused with UA resulted in hyperglycaemia, hyperinsulinaemia, hypertriglyceridaemia and hypercholesterolaemia and increase in insulin resistance in recipients when compared with recipients infused with serum from donors perfused with distilled water.

The present study confirms that UA and 1-MUA in the bladder produce features of metabolic syndrome and could be the result of an unknown humoral factor released from the bladder mucosa.