High-fat and high-sucrose diet leads to muscle loss and bladder dysfunction in rat

Wada N1, Abe N1, Miyauchi K1, Kakizaki H1

Research Type

Pure and Applied Science / Translational

Abstract Category

Anatomy / Biomechanics

Best in Category Prize: Anatomy / Biomechanics
Abstract 247
Pure and Applied Science
Scientific Podium Short Oral Session 29
Friday 29th September 2023
09:15 - 09:22
Room 104CD
Animal Study Detrusor Hypocontractility Pathophysiology Underactive Bladder Overactive Bladder
1. Asahikawa Medical University
Presenter
Links

Abstract

Hypothesis / aims of study
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.
Study design, materials and methods
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.
Results
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.
Interpretation of results
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.
Concluding message
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.
Figure 1 Representative cystometry traces in a rat fed on normal diet (A) and HFS diet (B).
Figure 2 Analyses of the urodynamic parameters in rats fed on normal and HFS diets. N = 10 in Group N and N = 9 in Group HFS.
References
  1. Gatineau E, et al. J Nutr. 2015;145: 923-30
  2. Collins KH, et al. J Orthop Res. 2016; 34: 2069-2078.
  3. Majima T, et al. Neurourol Urodyn. 2019; 38: 1417-1422
Disclosures
Funding JSPS KAKENHI Grant Number JP-19K18602 Clinical Trial No Subjects Animal Species Rat Ethics Committee Asahikawa Medical University Institutional Reviewer Board: No. 20018
Citation

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

23/11/2024 15:45:00