Glutamine in suppression of lipopolysaccharide-induced piglet intestinal inflammation: The crosstalk between AMPK activation and mitochondrial function

Liuqin He; Xihong Zhou; Ziping Wu; Yanzhong Feng; Di Liu; Tiejun Li; Yulong Yin

doi:10.1016/j.aninu.2022.03.001

Glutamine in suppression of lipopolysaccharide-induced piglet intestinal inflammation: The crosstalk between AMPK activation and mitochondrial function

Liuqin He
, Xihong Zhou
, Ziping Wu
, Yanzhong Feng
, Di Liu
, Tiejun Li^*
, Yulong Yin^*

^*Corresponding author for this work

School of Biological Sciences

Research output: Contribution to journal › Article › peer-review

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Abstract

The study was conducted to investigate the regulatory mechanism of glutamine (Gln) on intestinal inflammation in an lipopolysaccharide ( LPS)-induced in vivo and in vitro models. Piglets ( = 8) weaned at 21 d of age were fed a basal diet (control and LPS groups) or 1% Gln diet (Gln + LPS group) ad libitum for 4 weeks. On d 22, 24, 26 and 28, piglets in the LPS and Gln + LPS groups were intraperitoneally injected with LPS. Intestinal porcine epithelial cells (IPEC-J2) ( = 6) induced by LPS were used to assess related mechanisms and compound C was used to inhibit adenosine 5'-monophosphate-activated protein kinase (AMPK) activity. Our current results showed that compared with the LPS treatment, the Gln + LPS treatment had better growth performance and greater villus height ( < 0.05), and the Gln + LPS treatment reduced the rate of diarrhea by 6.4% ( < 0.05); the Gln + LPS treatment decreased serum tumor necrosis factor (TNF-ɑ), interleukin-6 (IL-6), K , cortisol and insulin levels, whereas increased ( < 0.05) serum immunoglobulin M and epidermal growth factor levels; the Gln + LPS treatment increased ( < 0.05) the expression of aquaporins and AMPK pathway-associated targets in the jejunum and ileum of piglets, whereas decreased the expression of ion transporters ( < 0.05). The in vitro results showed that 4 mmol/L Gln administration could inhibit ( < 0.05) cell apoptosis and interleukin-1β (IL-1β), IL-6 and TNF-ɑ secretion in LPS-induced IPEC-J2 cells, promote ( < 0.05) mitochondrial respiratory metabolism and increase ( < 0.05) the number of mitochondria and mitochondrial membrane potential. The activity of AMPK was elevated by 70% to 300% in Gln-treated IPEC-J2 cells under LPS challenge or normal conditions. Our results indicate that pre-administration of Gln to piglets suppresses intestinal inflammation by modulating the crosstalk between AMPK activation and mitochondrial function.

Original language	English
Pages (from-to)	137-147
Journal	Animal Nutrition
Volume	10
Early online date	26 Mar 2022
DOIs	https://doi.org/10.1016/j.aninu.2022.03.001
Publication status	Published - Sept 2022

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Glutamine in suppression of lipopolysaccharide-induced piglet intestinal inflammation: The crosstalk between AMPK activation and mitochondrial function
Copyright 2022 the authors. This is an open access article published under a Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits distribution and reproduction for non-commercial purposes, provided the author and source are cited.
Final published version, 3.07 MBLicence: CC BY-NC-ND

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@article{01f4b06c36aa4c3b8c59c30080e2bd57,

title = "Glutamine in suppression of lipopolysaccharide-induced piglet intestinal inflammation: The crosstalk between AMPK activation and mitochondrial function",

abstract = "The study was conducted to investigate the regulatory mechanism of glutamine (Gln) on intestinal inflammation in an lipopolysaccharide ( LPS)-induced in vivo and in vitro models. Piglets ( = 8) weaned at 21 d of age were fed a basal diet (control and LPS groups) or 1\% Gln diet (Gln + LPS group) ad libitum for 4 weeks. On d 22, 24, 26 and 28, piglets in the LPS and Gln + LPS groups were intraperitoneally injected with LPS. Intestinal porcine epithelial cells (IPEC-J2) ( = 6) induced by LPS were used to assess related mechanisms and compound C was used to inhibit adenosine 5'-monophosphate-activated protein kinase (AMPK) activity. Our current results showed that compared with the LPS treatment, the Gln + LPS treatment had better growth performance and greater villus height ( < 0.05), and the Gln + LPS treatment reduced the rate of diarrhea by 6.4\% ( < 0.05); the Gln + LPS treatment decreased serum tumor necrosis factor (TNF-ɑ), interleukin-6 (IL-6), K , cortisol and insulin levels, whereas increased ( < 0.05) serum immunoglobulin M and epidermal growth factor levels; the Gln + LPS treatment increased ( < 0.05) the expression of aquaporins and AMPK pathway-associated targets in the jejunum and ileum of piglets, whereas decreased the expression of ion transporters ( < 0.05). The in vitro results showed that 4 mmol/L Gln administration could inhibit ( < 0.05) cell apoptosis and interleukin-1β (IL-1β), IL-6 and TNF-ɑ secretion in LPS-induced IPEC-J2 cells, promote ( < 0.05) mitochondrial respiratory metabolism and increase ( < 0.05) the number of mitochondria and mitochondrial membrane potential. The activity of AMPK was elevated by 70\% to 300\% in Gln-treated IPEC-J2 cells under LPS challenge or normal conditions. Our results indicate that pre-administration of Gln to piglets suppresses intestinal inflammation by modulating the crosstalk between AMPK activation and mitochondrial function.",

author = "Liuqin He and Xihong Zhou and Ziping Wu and Yanzhong Feng and Di Liu and Tiejun Li and Yulong Yin",

year = "2022",

month = sep,

doi = "10.1016/j.aninu.2022.03.001",

language = "English",

volume = "10",

pages = "137--147",

journal = "Animal Nutrition",

issn = "2405-6545",

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T1 - Glutamine in suppression of lipopolysaccharide-induced piglet intestinal inflammation: The crosstalk between AMPK activation and mitochondrial function

AU - He, Liuqin

AU - Zhou, Xihong

AU - Wu, Ziping

AU - Feng, Yanzhong

AU - Liu, Di

AU - Li, Tiejun

AU - Yin, Yulong

PY - 2022/9

Y1 - 2022/9

N2 - The study was conducted to investigate the regulatory mechanism of glutamine (Gln) on intestinal inflammation in an lipopolysaccharide ( LPS)-induced in vivo and in vitro models. Piglets ( = 8) weaned at 21 d of age were fed a basal diet (control and LPS groups) or 1% Gln diet (Gln + LPS group) ad libitum for 4 weeks. On d 22, 24, 26 and 28, piglets in the LPS and Gln + LPS groups were intraperitoneally injected with LPS. Intestinal porcine epithelial cells (IPEC-J2) ( = 6) induced by LPS were used to assess related mechanisms and compound C was used to inhibit adenosine 5'-monophosphate-activated protein kinase (AMPK) activity. Our current results showed that compared with the LPS treatment, the Gln + LPS treatment had better growth performance and greater villus height ( < 0.05), and the Gln + LPS treatment reduced the rate of diarrhea by 6.4% ( < 0.05); the Gln + LPS treatment decreased serum tumor necrosis factor (TNF-ɑ), interleukin-6 (IL-6), K , cortisol and insulin levels, whereas increased ( < 0.05) serum immunoglobulin M and epidermal growth factor levels; the Gln + LPS treatment increased ( < 0.05) the expression of aquaporins and AMPK pathway-associated targets in the jejunum and ileum of piglets, whereas decreased the expression of ion transporters ( < 0.05). The in vitro results showed that 4 mmol/L Gln administration could inhibit ( < 0.05) cell apoptosis and interleukin-1β (IL-1β), IL-6 and TNF-ɑ secretion in LPS-induced IPEC-J2 cells, promote ( < 0.05) mitochondrial respiratory metabolism and increase ( < 0.05) the number of mitochondria and mitochondrial membrane potential. The activity of AMPK was elevated by 70% to 300% in Gln-treated IPEC-J2 cells under LPS challenge or normal conditions. Our results indicate that pre-administration of Gln to piglets suppresses intestinal inflammation by modulating the crosstalk between AMPK activation and mitochondrial function.

AB - The study was conducted to investigate the regulatory mechanism of glutamine (Gln) on intestinal inflammation in an lipopolysaccharide ( LPS)-induced in vivo and in vitro models. Piglets ( = 8) weaned at 21 d of age were fed a basal diet (control and LPS groups) or 1% Gln diet (Gln + LPS group) ad libitum for 4 weeks. On d 22, 24, 26 and 28, piglets in the LPS and Gln + LPS groups were intraperitoneally injected with LPS. Intestinal porcine epithelial cells (IPEC-J2) ( = 6) induced by LPS were used to assess related mechanisms and compound C was used to inhibit adenosine 5'-monophosphate-activated protein kinase (AMPK) activity. Our current results showed that compared with the LPS treatment, the Gln + LPS treatment had better growth performance and greater villus height ( < 0.05), and the Gln + LPS treatment reduced the rate of diarrhea by 6.4% ( < 0.05); the Gln + LPS treatment decreased serum tumor necrosis factor (TNF-ɑ), interleukin-6 (IL-6), K , cortisol and insulin levels, whereas increased ( < 0.05) serum immunoglobulin M and epidermal growth factor levels; the Gln + LPS treatment increased ( < 0.05) the expression of aquaporins and AMPK pathway-associated targets in the jejunum and ileum of piglets, whereas decreased the expression of ion transporters ( < 0.05). The in vitro results showed that 4 mmol/L Gln administration could inhibit ( < 0.05) cell apoptosis and interleukin-1β (IL-1β), IL-6 and TNF-ɑ secretion in LPS-induced IPEC-J2 cells, promote ( < 0.05) mitochondrial respiratory metabolism and increase ( < 0.05) the number of mitochondria and mitochondrial membrane potential. The activity of AMPK was elevated by 70% to 300% in Gln-treated IPEC-J2 cells under LPS challenge or normal conditions. Our results indicate that pre-administration of Gln to piglets suppresses intestinal inflammation by modulating the crosstalk between AMPK activation and mitochondrial function.

U2 - 10.1016/j.aninu.2022.03.001

DO - 10.1016/j.aninu.2022.03.001

M3 - Article

SN - 2405-6545

VL - 10

SP - 137

EP - 147

JO - Animal Nutrition

JF - Animal Nutrition

ER -

Glutamine in suppression of lipopolysaccharide-induced piglet intestinal inflammation: The crosstalk between AMPK activation and mitochondrial function

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