[Objective]Appetite is the most important factor affecting feed intake,multiple signals from central and peripheral sources can regulate feeding via the hypothalamic appetite center,and the intestine-brain axis plays an important role in appetite regulation in animals.This study aims to reveal the mechanism of intestine-brain axis in mediating 3-indolepropionic acid in regulating feed intake of animals,which is of high reference value for improving feed intake of animals.[Method]Twenty one 8-week-old C57BL/6J male mice were used as test subjects.The effects of different concentrations of 3-indolepropionic acid and normal saline on feed intake and body weight gain of mice were detected and analyzed respectively.Subsequently,techniques such as subdiaphragmatic vagotomy,c-Fos immunofluorescence and pharmacogenetics were used to reveal the neural circuitry of 3-indolepropionic acid in regulating the excitability of neurons in the nucleus tractus solitarius via the vagus nerve.[Result](1)Compared with the control group,10 mg/kg of 3-indolepropionic acid significantly increased the feed intake of mice for 3 h(P<0.05);3-indolepropionic acid increased the feed intake of mice through the activation of solitary tract nucleus(SCTN)neurons(P<0.01),and chemogenetic inhibition of the SCTN neurons eliminated the feeding-promoting effect of 3-indolepropionic acid;(2)3-Indolepropionic acid activated NG neurons through intestinal vagus nerve(P<0.001).Subphrenic vagotomy or chemical genetic activation of NG ganglion could eliminate the effect of 3-Indolepropionic acid on food intake.[Conclusion]3-indolepropionic acid activates solitary tract nucleus neurons through intestinal vagal neurotransmission,thereby increasing food intake in animals.
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