关键词：
Carbohydrate oxidation impairment;Flaxseed oil;Muscle atrophy;Protein kinase B/Forkhead box O signalling pathways;Toll-like receptor 4/nucleotide-binding oligomerisation domain protein signalling pathway
摘要：
<jats:title>Abstract</jats:title><jats:p>Flaxseed oil is rich in α-linolenic acid (ALA), which is the metabolic precursor of EPA and DHA. The present study investigated the effect of flaxseed oil supplementation on lipopolysaccharide (LPS)-induced muscle atrophy and carbohydrate oxidation impairment in a piglet model. Twenty-four weaned pigs were used in a 2 × 2 factorial experiment including dietary treatment (5 % maize oil<jats:italic>v</jats:italic>. 5 % flaxseed oil) and LPS challenge (saline<jats:italic>v</jats:italic>. LPS). On day 21 of treatment, the pigs were injected intraperitoneally with 100 μg/kg body weight LPS or sterile saline. At 4 h after injection, blood, gastrocnemius muscle and longissimus dorsi muscle were collected. Flaxseed oil supplementation increased ALA, EPA, total<jats:italic>n</jats:italic>-3 PUFA contents, protein:DNA ratio and pyruvate dehydrogenase complex quantity in muscles (<jats:italic>P</jats:italic>< 0·05). In addition, flaxseed oil reduced mRNA expression of toll-like receptor (TLR) 4 and nucleotide-binding oligomerisation domain protein (NOD) 2 and their downstream signalling molecules in muscles and decreased plasma concentrations of TNF-<jats:italic>α</jats:italic>, IL-6 and IL-8, and mRNA expression of TNF-<jats:italic>α</jats:italic>, IL-1<jats:italic>β</jats:italic>and IL-6 (<jats:italic>P</jats:italic>< 0·05). Moreover, flaxseed oil inclusion increased the ratios of phosphorylated protein kinase B (Akt) 1:total Akt1 and phosphorylated Forkhead box O (FOXO) 1:total FOXO1 and reduced mRNA expression of FOXO1, muscle RING finger (MuRF) 1 and pyruvate dehydrogenase kinase 4 in muscles (<jats:italic>P</jats:italic>< 0·05). These results suggest that flaxseed oil might have a positive effect on alleviating muscle protein loss and carbohydrates oxidation impairment induced by LPS challenge through regulation of the TLR4/NOD and Akt/FOXO signalling pathways.</jats:p>
作者机构：
[程铭; 焦文佳; 陶冶; 夏廉臣; 王雪晖] College of Food science and Engineering, Wuhan Polytechnic University, Wuhan, 430023, China;Grain and Oil Resources Comprehensive Exploitation and Engineering Technology Research Center of State Administration of Grain, Wuhan, 430023, China;[王春维] College of Food science and Engineering, Wuhan Polytechnic University, Wuhan, 430023, China<&wdkj&>Grain and Oil Resources Comprehensive Exploitation and Engineering Technology Research Center of State Administration of Grain, Wuhan, 430023, China
通讯机构：
College of Food science and Engineering, Wuhan Polytechnic University, Wuhan, China
摘要：
<jats:title>Abstract</jats:title><jats:p>This study was conducted to evaluate whether medium-chain TAG (MCT) could alleviate <jats:italic>Escherichia coli</jats:italic> lipopolysaccharide (LPS)-induced intestinal injury by regulating intestinal epithelial inflammatory response, as well as necroptosis. A total of twenty-four weanling piglets were randomly allotted to one of four treatments in a 2×2 factorial arrangement including diet type (5 % maize oil <jats:italic>v</jats:italic>. 4 % MCT+1 % maize oil) and immune stress (saline <jats:italic>v</jats:italic>. <jats:italic>E. coli</jats:italic> LPS). The piglets were fed diets containing maize oil or MCT for 21 d. On 21 d, piglets were injected intraperitoneally with saline or LPS. The blood and intestinal samples were collected at 4 h post injection. Supplementation with MCT improved intestinal morphology, digestive and barrier function, indicated by increased jejunal villus height, increased jejunal and ileal disaccharidases (sucrase and maltase) activities, as well as enhanced protein expression of claudin-1. Furthermore, the protein expression of heat-shock protein 70 in jejunum and the concentration of TNF-<jats:italic>α</jats:italic> in plasma were reduced in the piglets fed diets supplemented with MCT. In addition, MCT down-regulated the mRNA expression of toll-like receptor 4 (TLR4) and nucleotide-binding oligomerisation domain proteins (NOD) signalling-related genes in jejunum and ileum. Finally, MCT inhibited jejunal and ileal enterocyte necroptosis indicated by suppressed mRNA expression of the receptor-interacting protein 3 and mixed-lineage kinase domain-like protein. These results indicate that MCT supplementation may be closely related to inhibition of TLR4, NOD and necroptosis signalling pathways and concomitant improvement of intestinal integrity under an inflammatory condition.</jats:p>
作者机构：
[彭凯迪; 程思; 李奥; 程熠娜] School of Food Science And Engineering, Wuhan Polytechnic University, Wuhan, 430023, China;Key Laboratory of Hubei Province for Agricultural Products Processing and Transformation, Wuhan, 430023, China;Key Laboratory for Mass Cereals and Oils Further Processing Built by both Education Ministry and Province Ministry, Wuhan, 430023, China;[祝爱侠] School of Food Science And Engineering, Wuhan Polytechnic University, Wuhan, 430023, China<&wdkj&>Key Laboratory of Hubei Province for Agricultural Products Processing and Transformation, Wuhan, 430023, China;[王春维] School of Food Science And Engineering, Wuhan Polytechnic University, Wuhan, 430023, China<&wdkj&>Key Laboratory for Mass Cereals and Oils Further Processing Built by both Education Ministry and Province Ministry, Wuhan, 430023, China
通讯机构：
School of Food Science And Engineering, Wuhan Polytechnic University, Wuhan, China
摘要：
Stress causes intestinal inflammation and barrier dysfunction. Corticotrophin-releasing factor (CRF)/CRF receptor (CRFR) signaling pathway has been shown to be important for stress-induced intestinal mucosal alteration. L-Asparagine (ASN) is a powerful stimulator of ornithine decarboxylase and cell proliferation in a variety of cell types, including colonic cells. In the present study, we investigated whether dietary ASN supplementation could alleviate the damage of intestinal barrier function caused by LPS through modulation of CRF/CRFR signaling pathway. Twenty-four weaned pigs were randomly divided into one of four treatments: (1) non-challenged control; (2) Escherichia coli LPS challenged control; (3) LPS + 0.5% ASN; (4) LPS + 1.0% ASN. LPS stress induced villous atrophy, intestinal morphology disruption and decreased claudin-1 expression. ASN supplementation increased intestinal claudin-1 protein expression and alleviated villous atrophy and intestinal morphology impairment caused by LPS stress. In addition, ASN supplementation increased the number of intestinal intraepithelial lymphocytes and reversed the elevations of intestinal mast cell number and neutrophil number induced by LPS stress. Moreover, ASN decreased the mRNA expression of intestinal CRF, glucocorticoid receptors and tryptase. These results indicate that ASN attenuates intestinal barrier dysfunction induced by LPS stress, and regulates CRF/CRFR1 signaling pathway and mast cell activation.
