High-fat diet feeding reduced smooth muscle contractility and increasing tissue programmed death activity in rats bladder tissue.

purposeHigh-fat diet (HFD)-induced metabolic disturbances are recognized risk factors for bladder dysfunction, yet the underlying mechanisms remain incompletely understood.

methodsTwelve male Wistar rats were allocated to normal diet (ND) or HFD groups for 12 weeks. Physiological parameters, cystometry, and detrusor muscle contractility assays were performed. Histological analyses assessed vascular remodeling and fibrosis, while immunohistochemistry and western blotting evaluated programmed cell death pathways and receptor expression.

resultsHFD-fed rats exhibited significant body weight gain, hyperlipidemia, and increased baseline bladder pressure. Detrusor strips showed diminished contractility in response to KCl and carbachol but preserved ATP-induced responses. Histology revealed arteriosclerotic vascular changes and increased collagen deposition. Programmed cell death markers for apoptosis, pyroptosis, and autophagy were upregulated, alongside increased expression of the P2X₂ purinergic receptor, while the levels of muscarinic acetylcholine receptors M2 and M3 and the P2X₃ purinergic receptors remained unchanged.

conclusionChronic HFD feeding induces bladder dysfunction through smooth muscle impairment, fibrotic remodeling, and activation of multiple programmed cell death pathways, with compensatory enhancement of purinergic signaling via P2X₂ receptors. These findings provide mechanistic insight into metabolic syndrome-related bladder disorders and identify potential therapeutic targets.