Several previous studies in rats demonstrated that high-fat/high-sucrose (HFS) diet led to dynamic structural and inflammatory alterations of the skeletal muscle and accelerates the progression of sarcopenia by altering the postprandial stimulation of muscle protein synthesis [1,2]. Changes in the lower urinary tract function of these animals are expected; however, this lacks information. The structural and inflammatory alterations of the skeletal muscle may induce general or local oxidative stress reaction following ischemic change. We hypothesized that oxidative stress and ischemic change in the pelvis or the bladder in animals fed on HFS diet would induce bladder dysfunction. Thus, we investigated the change in the skeletal muscles and bladder function in rats fed on HFS diet.

Twelve-week SD female rats were used and fed on normal (Group N) or HFS (Group HFS) diet for 12 weeks. Urodynamic investigation under awake conditions and pharmacologic in vitro studies were performed. We measured gastrocnemius and tibialis muscle weight, and the protein concentration in both muscles. Hypoxia-inducible factor (HIF)-1α and 8-hydroxy-2’-deoxyguanosine (8-OHdG) in the bladder were assayed.

Absolute and relative gastrocnemius muscle weights were significantly lower in Group HFS. The protein concentration of gastrocnemius muscle in Group HFS was significantly lower than in Group N. Bladder absolute weights and relative weights were also significantly lower in Group HFS than in Group N. Urodynamic investigations showed the significantly shorter inter-contraction intervals and lower maximal voiding pressure  in Group HFS compared with Group N (Figure 1 and 2). Contractile responses of bladder strips to electrical field stimulation and carbachol were significantly lower in Group HFS than in Group N. HIF1α and 8OHdG in the bladder muscle were significantly higher in Group HFS compared with Group N.

This study demonstrated that HFS diet led to loss of the gastrocnemius muscle, voiding interval shortening, and bladder contractile force reduction in rats. Because the HIF1α and 8OHdG levels in the bladder muscle were increased, oxidative stress following bladder ischemia seemed to underlie these alterations of bladder function. HFS diet resulted in both skeletal muscle loss and bladder dysfunction similar to detrusor hyperreflexia with impaired contractility, which is most common in the elderly. A clinical study also showed that psoas muscle volume was positively associated with bladder contractility [3]. It is speculated that skeletal muscle loss is indirectly involved in the development of bladder dysfunction through bladder ischemia and oxidative stress in the pelvis.

In conclusion, this is the preliminary but the first attempt to elucidate the alterations of bladder function in HFS diet rats. HFS diet reduced bladder capacity and contractility with gastrocnemius muscle loss in rats. In addition, it led to the development of lower urinary tract dysfunction that is similar, at least in part, to detrusor hyperreflexia with impaired contractility.

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Collins KH, et al. J Orthop Res. 2016; 34: 2069-2078.
Majima T, et al. Neurourol Urodyn. 2019; 38: 1417-1422

Continence 7S1 (2023) 100965
DOI: 10.1016/j.cont.2023.100965