title: Dietary supplementation of aspartate enhances intestinal integrity and energy status in weanling piglets after lipopolysaccharide challenge.
abstract: The intestine has a high requirement for ATP to support its integrity, function and health, and thus, energy deficits in the intestinal mucosa may play a critical role in intestinal injury. Aspartate (Asp) is one of the major sources of ATP in mammalian enterocytes via mitochondrial oxidation. We hypothesized that dietary supplementation of Asp could attenuate lipopolysaccharide (LPS)-induced intestinal damage via modulation of intestinal energy status. Twenty-four weanling piglets were allotted to one of four treatments: (1) nonchallenged control, (2) LPS-challenged control, (3) LPS+0.5% Asp treatment, and (4) LPS+1.0% Asp treatment. On day 19, pigs were injected with saline or LPS. At 24 h postinjection, pigs were killed and intestinal samples were obtained. Asp attenuated LPS-induced intestinal damage indicated by greater villus height and villus height/crypt depth ratio as well as higher RNA/DNA and protein/DNA ratios. Asp improved intestinal function indicated by increased intestinal mucosal disaccharidase activities. Asp also improved intestinal energy status indicated by increased ATP, ADP and total adenine nucleotide contents, adenylate energy charge and decreased AMP/ATP ratio. In addition, Asp increased the activities of tricarboxylic acid cycle key enzymes including citrate synthase, isocitrate dehydrogenase and alpha-oxoglutarate dehydrogenase complex. Moreover, Asp down-regulated mRNA expression of intestinal AMP-activated protein kinase α1 (AMPKα1), AMPKα2, silent information regulator 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1α) and decreased intestinal AMPKα phosphorylation. These results indicate that Asp may alleviate LPS-induced intestinal damage and improve intestinal energy status.
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China.
authors.forename: Dingan
authors.initials: D
authors.lastname: Pi
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China. Electronic address: yulanflower@126.com.
authors.forename: Yulan
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China.
authors.forename: Haifeng
authors.initials: H
authors.lastname: Shi
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China.
authors.forename: Shuang
authors.initials: S
authors.lastname: Li
authors.affiliation: Laboratory of Developmental Nutrition, Department of Animal Science, North Carolina State University, Raleigh, NC 27695, USA.
authors.forename: Jack
authors.initials: J
authors.lastname: Odle
authors.affiliation: Laboratory of Developmental Nutrition, Department of Animal Science, North Carolina State University, Raleigh, NC 27695, USA.
authors.forename: Xi
authors.initials: X
authors.lastname: Lin
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China.
authors.forename: Huiling
authors.initials: H
authors.lastname: Zhu
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Chen
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China.
authors.forename: Yongqing
authors.initials: Y
authors.lastname: Hou
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China.
authors.forename: Weibo
authors.initials: W
authors.lastname: Leng
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D004247:DNA / Q000378:metabolism; D019587:Dietary Supplements; D006655:Histone Deacetylases / Q000235:genetics; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism*; D007422:Intestines / Q000187:drug effects*; D043322:Lactase / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D010766:Phosphorylation / Q000187:drug effects; D011506:Proteins / Q000378:metabolism; D013393:Sucrase / Q000378:metabolism; D013552:Swine; D014157:Transcription Factors / Q000235:genetics; D014886:Weaning
chemical_list: D008070:Lipopolysaccharides; D011506:Proteins; D014157:Transcription Factors; D001224:Aspartic Acid; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D004247:DNA; D055372:AMP-Activated Protein Kinases; D043322:Lactase; D013393:Sucrase; D006655:Histone Deacetylases
keywords: Aspartate; Energy status; Intestine; Lipopolysaccharide; Weanling piglets