Animal Nutrition (Sep 2022)
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 Escherichia coli lipopolysaccharide (E. coli LPS)-induced in vivo and in vitro models. Piglets (n = 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 E. coli LPS. Intestinal porcine epithelial cells (IPEC-J2) (n = 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 (P < 0.05), and the Gln + LPS treatment reduced the rate of diarrhea by 6.4% (P < 0.05); the Gln + LPS treatment decreased serum tumor necrosis factor (TNF-ɑ), interleukin-6 (IL-6), K+, cortisol and insulin levels, whereas increased (P < 0.05) serum immunoglobulin M and epidermal growth factor levels; the Gln + LPS treatment increased (P < 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 (P < 0.05). The in vitro results showed that 4 mmol/L Gln administration could inhibit (P < 0.05) cell apoptosis and interleukin-1β (IL-1β), IL-6 and TNF-ɑ secretion in LPS-induced IPEC-J2 cells, promote (P < 0.05) mitochondrial respiratory metabolism and increase (P < 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.
