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中华肥胖与代谢病电子杂志

中华肥胖与代谢病电子杂志 ›› 2022, Vol. 08 ›› Issue (02) : 93 -96. doi: 10.3877/cma.j.issn.2095-9605.2022.02.004

论著

小肠电刺激减少肥胖大鼠进食时间
叶晓玲1, 张宇2, 万新月3,†()   
  1. 1. 430060　武汉，武汉大学人民医院消化内科；310000　杭州，浙江大学医学院附属第一医院超声影像科
    2. 430060　武汉，武汉大学人民医院消化内科；450003　郑州，河南省人民医院消化内科
    3. 430060　武汉，武汉大学人民医院消化内科
  • 收稿日期:2022-01-30 出版日期:2022-05-30
  • 通信作者: 万新月
  • 基金资助:
    国家自然科学基金青年项目(81800481)

The eating duration was reduced by intestinal electrical stimulation in obese rats

Xiaoling Ye1, Yu Zhang2, Xinyue Wan3,†()   

  1. 1. Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Department of Ultrasound imaging, The First Affiliated Hospital of Zhejiang University Medical College, Hangzhou 310000, China
    2. Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Department of Gastroenterology, Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, Zhengzhou 450003, China
    3. Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, China
  • Received:2022-01-30 Published:2022-05-30
  • Corresponding author: Xinyue Wan
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引用本文：

叶晓玲, 张宇, 万新月. 小肠电刺激减少肥胖大鼠进食时间[J]. 中华肥胖与代谢病电子杂志, 2022, 08(02): 93-96.

Xiaoling Ye, Yu Zhang, Xinyue Wan. The eating duration was reduced by intestinal electrical stimulation in obese rats[J]. Chinese Journal of Obesity and Metabolic Diseases(Electronic Edition), 2022, 08(02): 93-96.

目的

通过观察小肠电刺激（IES）对肥胖大鼠进食模式的影响，初步探索小肠电刺激的减重机制。

方法

16只饮食诱导肥胖大鼠（DIO）被纳入试验。使用BioDAQ系统记录4组不同刺激时长（IES-0h，IES-1h，IES-6h和IES-12h）下DIO大鼠的进食模式。使用酶联免疫吸附法（ELISA）检测DIO大鼠餐后血清胰高血糖素样肽-1（GLP-1）及瘦素（Leptin）的表达水平。

结果

4组日均摄食量分别为（22.3±2.9）g、（21.9±3.7）g、（19.6±4.3）g和（17.5±5.1）g，呈现刺激时长依赖性下降趋势；大鼠日均进食次数无明显差异，但日均进食时间明显缩短。IES-12h组为（112.8±50.3）min对比对照组IES-0h组（147.9±52.1）min明显缩短（P<0.01）。DIO大鼠接受IES刺激1 h后餐后血清GLP-1对比对照组明显升高，而两组瘦素表达水平无差异。

结论

小肠电刺激通过减少DIO大鼠进食时间来减重，而GLP-1可能在其中发挥了作用。

关键词: 小肠电刺激, 肥胖, 胰高血糖素样肽-1, 机制
Objective

Investigating the mechanism of intestinal electrical stimulation (IES) induced weight loss in obese rats by observing the changes of meal pattern.

Methods

Sixteen diet-induced obese rats (DIO) were used in the experiment. The BioDAQ system was used to record events of food intake. And the changes of meal pattern of obese rats with different stimulation duration (0 h, 1 h, 6 h and 12 h) were compared. Lastly, the levels of serum glucagon-like peptide-1 (GLP-1) and Leptin were tested by enzyme-linked immunosorbent assay (ELISA).

Results

The average daily food intake with four different stimulation duration were (22.3±2.9) g, (21.9±3.7) g, (19.6±4.3) g and (17.5±5.1) g, respectively. This was a stimulation time-dependent downward trend. There was no significant difference in the average daily feeding times of rats, but the eating duration were significantly shortened, and the average eating duration of 12hours stimulation (IES-12h) was significantly shorter than that of IES-0h, (112.8±50.3) min vs.(147.9±52.1) min. When DIO rats received one hour stimulation, the level of postprandial serum GLP-1 was significantly higher than that of sham-IES, but there was no difference on the level of Leptin between the two groups.

Conclusions

IES caused the weight loss of obese rats by reducing the eating duration, and GLP-1 may play a role in it.

Key words: Intestinal electrical stimulation, Obesity, Glucagon-like peptide-1, Mechanism
表1 4组刺激时长下大鼠的进食模式情况
进食模式 分组
IES-0h IES-1h IES-6h IES-12h
平均进食次数 4.5±0.9 4.4±1.1 4.4±0.8 4.2±1.1
平均进食时间（min） 147.9±52.1 151.1±50.5 123.7±57.4* 112.8±50.3*
平均进食量（g） 22.3 ± 2.9 21.9 ± 3.7 19.6 ± 4.3* 17.5 ± 5.1*
图1 4组不同刺激时长下平均每小时进食量
图2 IES组和对照组肥胖大鼠餐前和餐后1 h GLP-1表达水平
图3 IES组和对照组肥胖大鼠餐前和餐后1 h leptin表达水平
[1]
Wang Y, Wang L, Qu W. New national data show alarming increase in obesity andnoncommunicable chronic diseases in China [J]. Eur J Clin Nutr, 2017, 71: 149.
[2]
黄梦真，黄韦歆，熊逸波, 等. 病态肥胖患者行减重手术术后镇痛效果研究 [J/CD]. 中华肥胖与代谢病电子杂志, 2021, 7(2): 81-85.
[3]
Tak YJ, Lee SY. Long-term efficacy and safety of anti-obesity treatment: where dowe stand? [J]. Curr Obes Rep, 2021, 10(1):14-30.
[4]
Fan CJ, Chien HL, Weiss MJ, et al. Minimally invasive versus open surgery in the Medicare population: a comparison of post-operative and economic outcomes [J]. SurgEndosc, 2018, 32(9):3874-3880.
[5]
Li SY, Chen JD. Pulse width-dependent effects of intestinal electrical stimulation for obesity: role of gastrointestinal motility and hormones [J]. Obes Surg, 2017, 27(1): 70-77.
[6]
Hasler WL. Intestinal electrical stimulation: a possible treatment for morbid obesity? [J]. Gastroenterology, 2005, 128(5):1523-1524.
[7]
Li SY, Zhu WJ, Zhang SJ, et al. Chronic intestinal electricalstimulation improves glucose intolerance and insulin resistance in diet-induced obesity rats [J]. Obesity, 2017, 25(6):1061-1068.
[8]
Li SY, Kim Y, Chen JD, et al. Intestinal electrical stimulation alters hypothalamicexpression of oxytocin and orexin and ameliorates diet-inducedobesity in rats [J]. Obes Surg, 2021, 31(4):1664-1672.
[9]
Liu S, Hou XH, Chen JD. Therapeutic potential of duodenal electrical stimulation for obesity: acute effects on gastric emptying and water intake [J]. Am JGastroenterol, 2005, 100(4):792-796.
[10]
Fonken LK, Workman JL, Walton JC, et al. Light at night increases body mass by shifting the time of food intake [J]. Proc Natl Acad Sci USA, 2010, 107(43):18664-18669.
[11]
Pathak V, Flatt PR, Irwin N. Cholecystokinin (CCK) and related adjunct peptide therapies for the treatment of obesity and type 2 diabetes [J]. Peptides, 2018, 100:229-235.
[12]
Seth M, Biswas R, Ganguly S. Leptin and obesity [J]. Physiol Int, 2020, 107(4): 455-468.
[13]
Grill HJ. A role for GLP-1 in treating hyperphagia and obesity[J].Endocrinol, 2020, 161(8):bqaa093.
[14]
Ye F, Liu Y, Li SY, et al. Hypoglycemic effects of intestinal electricalstimulation by enhancing nutrient-stimulated secretion of GLP-1 rats [J]. ObesSurg, 2018, 28(9): 2829-2835.
[15]
Schwartz A, Ort T, Kajekar R, et al. Electrical stimulation of the isolated rat intestine in the presence of nutrient stimulus enhances glucagon-like peptide-1 release [J]. Physiol Meas, 2010, 31(9):1147-1159.
[16]
Hira T, Pinyo J, Hara H.What is GLP-1 really doing in obesity? [J]. TrendsEndocrinol Metab, 2020, 31(2):71-80.
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