Πέμπτη 26 Μαΐου 2016

Effect of estrogen on visceral sensory function in a non-inflammatory colonic hypersensitivity rat model

Abstract

Background

Increased prevalence of functional gastrointestinal disorders in women and perimenstrually accentuated symptoms imply that sexual hormones play a crucial role in the pathogenesis of such syndromes. The aim of this study was to analyze the selective effect of estrogen on visceral sensitivity in gonadectomized female and male Lewis rats with or without prior treatment with butyrate enemas.

Methods

Following ovariectomy (OVX) or orchiectomy (ORX) estradiol pellets (E2-P) or sham pellets (Sham-P) were implanted. After treatment with butyrate (BUT) or saline (NaCl) enemas, colorectal distensions (CRD) were performed and the visceromotor reflex (VMR) to CRD was measured by electromyography.

Key Results

Gender did not influence VMR to CRD in gonadectomized animals. VMR in E2-P animals compared to Sham-P animals was increased (635 ± 32 μVs vs 470 ± 39 μVs; p = 0.002). Overall, instillation of butyrate enemas did not influence VMR to CRD. A comparison of CRD clusters showed that butyrate enemas in the E2-P animals resulted in a significant sensitization in both OVX and ORX animals. In female rats, sensitization was also caused by estrogen substitution alone.

Conclusion & Inferences

In our animal model, estrogen is a strong factor for an increase in visceral sensory function. Surprisingly, the treatment with butyrate alone did not evoke a general rise in VMR to CRD. Rats treated with butyrate enemas and under selective estrogen substitution developed visceral sensitization during the series of CRDs.

Thumbnail image of graphical abstract

To study the effect of sexual hormones on visceral nociception, the selective effect of estrogen on visceral sensitivity in gonadectomized female and male Lewis rats with or without prior treatment with butyrate enemas was studied. In our rat model, estrogen is a strong factor for an increase in visceral sensory function.



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