Roux-en-Y Gastrointestinal Bypass Promotes Activation of TGR5 and Peptide YY

G蛋白偶联胆汁酸受体 肽YY 胆汁酸 内分泌学 内科学 野生型 受体 基因剔除小鼠 免疫印迹 生物 医学 神经肽Y受体 生物化学 神经肽 突变体 基因
作者
Haojun Yang,Hanyang Liu,Yu Jiao,Jun Qian
出处
期刊:Endocrine, metabolic & immune disorders [Bentham Science Publishers]
卷期号:20 (8): 1262-1267 被引量:4
标识
DOI:10.2174/1871530320666200628024500
摘要

Background: G protein-coupled bile acid receptor (TGR5) is involved in a number of metabolic diseases. The aim of this study was to identify the role of TGR5 after Roux-en-Y gastric bypass (GBP). Methods: Wild type and TGR5 knockout mice (tgr5-/-) were fed a high-fat diet (HFD) to establish the obesity model. GBP was performed. The changes in body weight and food intake were measured. The levels of TGR5 and peptide YY (PYY) were evaluated by RT-PCR, Western blot, and ELISA. Moreover, the L-cells were separated from wild type and tgr5-/- mice. The levels of PYY in L-cells were evaluated by ELISA. Results: The body weights were significantly decreased after GBP in wild type mice (p<0.05), but not tgr5-/- mice (p>0.05). Food intake was reduced after GBP in wild type mice, but also not significantly affected in tgr5-/- mice (p>0.05). The levels of PYY were significantly increased after GBP compared with the sham group (p<0.05); however, in tgr5-/- mice the expression of PYY was not significantly affected (p>0.05). After INT-777 stimulation in L-cells obtained from murine intestines, the levels of PYY were significantly increased in L-cells tgr5+/+ (p<0.05). Conclusion: Our study suggests that GBP up-regulated the expression of TGR5 in murine intestines, and increased the levels of PYY, which further reduced food intake and decreased the body weight.

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