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[Role of orphan G protein-coupled receptor 55 in diabetic gastroparesis in mice.] [Article in Chinese]

LIN Xu-Hong, WEI Dan-Dan, WANG Hui-Chao, WANG Bin, BAI Chun-Yang, WANG Ya-Qiang, LI Guo-En, LI Hui-Ping, REN Xue-Qun*

1Department of Clinical Laboratory, Huaihe Hospital Affiliated to Henan University, Kaifeng 475000, China; 2Department of Nephrology, First Affiliated Hospital of Henan University, Kaifeng 475000, China; 3Department of Digestive Medicine, Huaihe Hospital Affiliated to Henan University, Kaifeng 475000, China; 4Department of General Surgery, Huaihe Hospital Affiliated to Henan University, Kaifeng 475000, China

Abstract

The aim of the present study was to explore the role of orphan G protein-coupled receptor 55 (GPR55) in diabetic gastroparesis (DG). Streptozotocin (STZ) was used to mimic the DG model, and the body weight and blood glucose concentration were tested 4 weeks after STZ injection (i.p.). Electrogastrogram and phenolsulfonphthalein test were used for detecting gastric emptying. Motilin (MTL), gastrin (GAS), vasoactive intestinal peptide (VIP), and somatostatin (SS) levels in plasma were determined using radioimmunology. Real-time PCR and Western blot were applied to identify the expression of GPR55 in gastric tissue, and immunohistochemistry was used to detect the distribution. The effect of lysophosphatidylinositol (LPI), an agonist of GPR55, was observed. STZ mice showed increased blood glucose concentration, lower body weight, decreased amplitude of slow wave, and delayed gastric emptying. LPI antagonized these effects of STZ. Compared to the control group, STZ caused significant decreases of MTL and GAS levels (P < 0.01), as well as increases of SS and VIP levels (P < 0.01). The changes of these hormones induced by STZ were counteracted when using LPI. GPR55 located in mice stomach, and it was up-regulated in DG. Although LPI showed no effects on the distribution and expression of GPR55 in normal mice, it could inhibit STZ-induced GPR55 up-regulation. These results suggest GPR55 is involved in the regulation of gastric movement of DG, and may serve as a new target of DG treatment. LPI, an agonist of GPR55, can protect against STZ-induced DG, and the mechanism may involve the change of GPR55 expression and modification of gastrointestinal movement regulating hormones.

Key words: G protein-coupled receptor 55; diabetic gastroparesis; lysophosphatidylinositol

Received: 2013-09-17  Accepted: 2013-11-07

Corresponding author: 任学群  E-mail: hhyyrxq@126.com

Citing This Article:

LIN Xu-Hong, WEI Dan-Dan, WANG Hui-Chao, WANG Bin, BAI Chun-Yang, WANG Ya-Qiang, LI Guo-En, LI Hui-Ping, REN Xue-Qun. [Role of orphan G protein-coupled receptor 55 in diabetic gastroparesis in mice.] [Article in Chinese]. Acta Physiol Sin 2014; 66 (3): 332-340 (in Chinese with English abstract).