title: Effects of α-ketoglutarate on energy status in the intestinal mucosa of weaned piglets chronically challenged with lipopolysaccharide.
abstract: The present study determined whether α-ketoglutarate (AKG) might affect the expression of AMP-activated protein kinase (AMPK) and energy status in the intestinal mucosa of piglets challenged with Escherichia coli lipopolysaccharide (LPS). A total of eighteen piglets (weaned at 21 d of age) were allocated to one of three treatments: (1) non-challenged (control); (2) LPS-challenged (LPS); (3) LPS+1 % AKG (LPS+AKG). Piglets in the control and LPS groups were fed a maize- and soyabean meal-based diet, and the LPS+AKG group was fed the basal diet supplemented with 1 % AKG. On days 10, 12, 14 and 16 of the trial, piglets in the LPS and LPS+AKG groups were challenged with LPS (80 μg/kg body weight), whereas piglets in the control group received the same volume of sterile saline. Pigs were euthanised 24 h after the last administration of LPS or saline to obtain intestinal mucosae for biochemical analysis. Compared with the control group, LPS administration decreased (P < 0·05) the oxidation of AKG, oleic acid, glutamine and glucose in enterocytes, decreased concentrations of ATP in the duodenal and jejunal mucosae and decreased adenylate energy charge (AMP:ATP ratio) in the jejunal and ileal mucosae. Additionally, LPS treatment reduced (P < 0·05) mucosal concentrations of phosphorylated AMPK in the jejunum and ileum as well as acetyl-CoA carboxylase in all segments of the small intestine. The adverse effects of LPS were reversed by AKG. Collectively, these results indicate that dietary supplementation with 1 % AKG beneficially modulates the AMPK signalling pathway to improve energy status in the small intestine of LPS-challenged piglets.
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, People's Republic of China. houyq777@yahoo.com.cn
authors.forename: Yongqing
authors.initials: Y
authors.lastname: Hou
authors.forename: Kang
authors.initials: K
authors.lastname: Yao
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Binying
authors.initials: B
authors.lastname: Ding
authors.forename: Dabo
authors.initials: D
authors.lastname: Fu
authors.forename: Yulan
authors.initials: Y
authors.lastname: Liu
authors.forename: Huiling
authors.initials: H
authors.lastname: Zhu
authors.forename: Jian
authors.initials: J
authors.lastname: Liu
authors.forename: Yongtang
authors.initials: Y
authors.lastname: Li
authors.forename: Ping
authors.initials: P
authors.lastname: Kang
authors.forename: Yulong
authors.initials: Y
authors.lastname: Yin
authors.forename: Guoyao
authors.initials: G
authors.lastname: Wu
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D019587:Dietary Supplements; D020895:Enterocytes / Q000378:metabolism*; D004926:Escherichia coli; D005260:Female; D005947:Glucose / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D007410:Intestinal Diseases / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D007421:Intestine, Small / Q000378:metabolism*; D007656:Ketoglutaric Acids / Q000494:pharmacology* / Q000627:therapeutic use; D008070:Lipopolysaccharides; D019301:Oleic Acid / Q000378:metabolism; D010084:Oxidation-Reduction; D010766:Phosphorylation; D015398:Signal Transduction / Q000187:drug effects; D013552:Swine; D014886:Weaning
chemical_list: D007656:Ketoglutaric Acids; D008070:Lipopolysaccharides; D005973:Glutamine; D019301:Oleic Acid; D000249:Adenosine Monophosphate; D000255:Adenosine Triphosphate; D055372:AMP-Activated Protein Kinases; D000103:Acetyl-CoA Carboxylase; D005947:Glucose