Disturbed Gastrointestinal Contractility in a Polycystic Ovary Syndrome Rat Model
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ORIGINAL ARTICLE
Disturbed Gastrointestinal Contractility in a Polycystic Ovary Syndrome Rat Model Kai‑Lee Wang1,2 · Shih‑Min Hsia3 · Paulus S. Wang2,4,5,6 · Po‑Han Lin3 Received: 12 September 2019 / Accepted: 5 December 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Background Polycystic ovary syndrome (PCOS), a common hormonal disorder in women, affects 4–18% of women of reproductive age worldwide. A higher prevalence of irritable bowel syndrome was found in women with PCOS. However, the effects and mechanism of PCOS on stomach and colon contractility remain unclear. Aims This study aims to evaluate the correlation between PCOS and gastrointestinal disorder. Methods Four-week-old female rats were subcutaneously implanted with pellets containing 7.5 mg of dihydrotestosterone for 13 weeks to create PCOS rat models. After vaginal smears, the estrus cycle stage was evaluated. Oral glucose tolerance test was performed after 90 days of treatment. All animals were killed at 17 weeks. The rats were fasted overnight and then anesthetized before decapitation, and the stomach fundus and colon were surgically removed and cultured in oxygenated Krebs solution. Acetylcholine and carbachol were used to evaluate the cholinergic system on contractility. Results The basal and stomach fundus responded with a reduced frequency and contractility in response to acetylcholine in the PCOS group. Moreover, no difference was found in the spontaneous stomach contractility induced by carbachol in both groups. Lower maximal colon muscle contractility was also found in response to acetylcholine stimulation in PCOS rats. Furthermore, lower maximal muscle contractility was found in response to extracellular calcium levels. MLC20 phosphorylation was also reduced in the gastrointestinal tissue in PCOS rats. Conclusions PCOS induces gastroparesis and reduces gastrointestinal muscle contractility. This effect is, at least partly, through reducing the responsiveness of acetylcholine and MLC20 phosphorylation. Keywords Polycystic ovary syndrome · Gastrointestinal contraction · Acetylcholine · Carbachol · Muscle contractility Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10620-019-06001-x) contains supplementary material, which is available to authorized users. * Kai‑Lee Wang [email protected]; [email protected] 1
Department of Nursing, Ching Kuo Institute of Management and Health, No. 336, Fuxsin Rd., Zhongshan Dist., Keelung City 20301, Taiwan, Republic of China
2
Department of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China
3
School of Nutrition and Health Sciences, Taipei Medical University, Taipei 11031, Taiwan, Republic of China
4
Department of Medical Research and Education, Taipei Veterans General Hospital, Taipei, Taiwan, Republic of China
5
PhD Program of Aging, College of Medicine, China Medical University, Taichung, Taiwan, Republic of China
6
Department of Biotechnolog
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