Diabetes induced decrease in detrusor smooth muscle force is associated with oxidative stress and overactivity of...

Area of Science:

• Urology
• Endocrinology
• Diabetology

Background:

• Diabetes mellitus is a common condition with numerous complications.
• Diabetic bladder dysfunction is a recognized complication, impacting bladder function.
• The underlying mechanisms, particularly smooth muscle contractility changes, require further elucidation.

Purpose of the Study:

• To investigate the association between diabetic-induced bladder dysfunction and decreased detrusor smooth muscle contractility.
• To determine if hyperglycemia-induced over-expression of aldose reductase (AR) and increased sorbitol production contribute to this dysfunction.
• To compare oxidative stress markers, specifically lipid peroxidation, in the detrusor smooth muscle of diabetic and normal rabbits.

Main Methods:

• Diabetes was induced in rabbits using alloxan; control groups included normal and sucrose-drinking rabbits.
• Detrusor smooth muscle tissue was isolated from rabbits six months post-diabetes induction.
• Analysis included force generation, lipid peroxidation (malondialdehyde), AR expression (RT-PCR), and sorbitol levels.

Main Results:

• Diabetic rabbits showed a 57% decrease in detrusor muscle force compared to controls.
• Bethanechol-induced force decreased by 40% in diabetic rabbits.
• Increased AR expression, sorbitol content, and lipid peroxidation products were observed in diabetic detrusor muscle.

Conclusions:

• Diabetes significantly reduces detrusor smooth muscle contractility.
• Increased sorbitol and lipid peroxides, linked to AR over-expression and polyol pathway activation, suggest a role in oxidative stress.
• These molecular changes likely contribute to the development of diabetic bladder dysfunction.