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Choline Alleviates Parenteral Nutrition–Associated Duodenal Motility Disorder in Infant Rats
Author(s) -
Zhu Jie,
Wu Yang,
Guo Yonggao,
Tang Qingya,
Lu Ting,
Cai Wei,
Huang Haiyan
Publication year - 2016
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607115583674
Subject(s) - choline , duodenum , endocrinology , medicine , betaine , parenteral nutrition , phosphocholine , motility , biology , chemistry , phospholipid , biochemistry , membrane , phosphatidylcholine , genetics
Background: Parenteral nutrition (PN) has been found to influence duodenal motility in animals. Choline is an essential nutrient, and its deficiency is related to PN‐associated organ diseases. Therefore, this study was aimed to investigate the role of choline supplementation in an infant rat model of PN‐associated duodenal motility disorder. Materials and Methods : Three‐week‐old Sprague‐Dawley male rats were fed chow and water (controls), PN solution (PN), or PN plus intravenous choline (600 mg/kg) (PN + choline). Rats underwent jugular vein cannulation for infusion of PN solution or 0.9% saline (controls) for 7 days. Duodenal oxidative stress status, concentrations of plasma choline, phosphocholine, and betaine and serum tumor necrosis factor (TNF)–α were assayed. The messenger RNA (mRNA) and protein expression of c‐Kit proto‐oncogene protein (c‐Kit) and membrane‐bound stem cell factor (mSCF) together with the electrophysiological features of slow waves in the duodenum were also evaluated. Results : Rats on PN showed increased reactive oxygen species; decreased total antioxidant capacity in the duodenum; reduced plasma choline, phosphocholine, and betaine; and enhanced serum TNF‐α concentrations, which were reversed by choline intervention. In addition, PN reduced mRNA and protein expression of mSCF and c‐Kit, which were inversed under choline administration. Moreover, choline attenuated depolarized resting membrane potential and declined the frequency and amplitude of slow waves in duodenal smooth muscles of infant rats induced by PN, respectively. Conclusion : The addition of choline to PN may alleviate the progression of duodenal motor disorder through protecting smooth muscle cells from injury, promoting mSCF/c‐Kit signaling, and attenuating impairment of interstitial cells of Cajal in the duodenum during PN feeding.