title: Effects of dietary glutamine on inflammatory mediator gene expressions in rats with streptozotocin-induced diabetes.
abstract: OBJECTIVE
  This study investigated the effects of glutamine (Gln) supplementation on gene expressions of inflammatory mediators and cytokines associated with T-helper cell type 17 (Th17) regulation in diabetic rats.
  
  
  METHODS
  There were one normal control group and two diabetic groups in this study. Rats in the normal control group were fed a regular chow diet. One diabetic group (DM) was fed a common semipurified diet, and the other diabetic group received a diet in which part of the casein was replaced by Gln (DM-Gln), which provided 25% of the total amino acid nitrogen for 8 wk. Diabetes was induced by an intraperitoneal injection of nicotinamide followed by streptozotocin. Rats with blood glucose levels exceeding 200 mg/dL were considered diabetic. Blood samples and blood mononuclear cells of the animals were collected at the end of the study for further analysis.
  
  
  RESULTS
  Gene expressions of transforming growth factor-β1 and interleukin-17A did not differ in blood mononuclear cells among the three groups. Expressions of interleukin-6, interleukin-23, monocyte chemotactic protein-1, and the receptor of the advanced glycated endproducts gene were higher in blood mononuclear cells and the ratio of reduced to oxidized glutathione was lower in erythrocytes in the DM group than in the normal control group. Messenger RNA expressions of these genes were lower, whereas the ratio of reduced to oxidized glutathione was higher in the DM-Gln group than in the DM group.
  
  
  CONCLUSIONS
  Supplemental dietary Gln increased the antioxidant potential and downregulated the expressions of inflammatory mediators. However, Th17 might not be an important involved pathway and the regulatory effect of Gln on Th17 immune response was not obvious in this animal model.
authors: School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan.
authors: Pei-Hsuan
authors: PH
authors: Tsai
authors: Chui-Li
authors: CL
authors: Yeh
authors: Jun-Jen
authors: JJ
authors: Liu
authors: Wan-Chun
authors: WC
authors: Chiu
authors: Sung-Ling
authors: SL
authors: Yeh
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D018932:Chemokine CCL2 / Q000097:blood / Q000235:genetics; D003921:Diabetes Mellitus, Experimental / Q000235:genetics* / Q000378:metabolism; D019587:Dietary Supplements; D004195:Disease Models, Animal; D015536:Down-Regulation; D019270:Fructosamine / Q000097:blood; D015870:Gene Expression / Q000187:drug effects*; D005973:Glutamine / Q000008:administration & dosage*; D007249:Inflammation / Q000235:genetics*; D018836:Inflammation Mediators / Q000378:metabolism*; D020381:Interleukin-17 / Q000097:blood / Q000235:genetics; D053759:Interleukin-23 / Q000097:blood / Q000235:genetics; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D009536:Niacinamide / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D058504:Th17 Cells / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000097:blood / Q000235:genetics
chemical_list: D001786:Blood Glucose; D018932:Chemokine CCL2; D018836:Inflammation Mediators; D020381:Interleukin-17; D053759:Interleukin-23; D015850:Interleukin-6; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; D005973:Glutamine; D009536:Niacinamide; D019270:Fructosamine