title: Parenteral nutrition administration leads to specific alterations in the expression of adipocytokines and peroxisome proliferator-activated receptors in a rat model.
abstract: BACKGROUND
  Similar to metabolic syndrome, parenteral nutrition (PN) administration has also been associated with biologic abnormalities of glucose and lipids. Such complications include hyperglycemia, hypertriglyceridemia, liver dysfunction, and hepatobiliary complications. Because metabolic syndrome has been associated with altered expression of adipocytokines, and peroxisome proliferator-activated receptors (PPARs), the present study hypothesized that PN would also lead to alterations in adipocytokines and related gene abundances.
  
  
  METHODS
  Male Wister rats received either intravenous (IV) saline and chow (control) or PN. To determine the contribution of lipids to metabolic changes, the following 2 PN groups were studied: PN with IV lipid (PN+L) and PN without lipid (PN-L). Rats were studied after 7 days.
  
  
  RESULTS
  A marked increase in hepatic glycogen staining was found in the PN-L group, and conversely, a marked increase in hepatic lipid staining was observed in the PN+L group. Both PN groups demonstrated a 30% increase in serum adiponectin levels in comparison to controls. In the liver, ACDC mRNA expression significantly increased (10%-20%), while ADIPOR1 expression significantly declined in the PN groups compared with controls. PPAR expression significantly declined (10%-30%) in the PN+L group compared with controls. In contrast to metabolic syndrome, PN+L led to a decrease in tumor necrosis factor α and interleukin 6 levels in the liver.
  
  
  CONCLUSIONS
  The study shows that PN led to specific alterations in the abundance of adipocytokines and PPARs. These changes give critical insight into many of the metabolic derangements in lipid metabolism, which patients may experience with PN.
authors.affiliation: Osaka University Graduate School of Medicine, Osaka, Japan. tazuyan@aol.com
authors.forename: Yuko
authors.initials: Y
authors.lastname: Tazuke
authors.forename: Daniel
authors.initials: D
authors.lastname: Teitelbaum
authors.forename: Masafumi
authors.initials: M
authors.lastname: Wasa
authors.forename: Masahiro
authors.initials: M
authors.lastname: Fukuzawa
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Iiboshi
authors.forename: Jiro
authors.initials: J
authors.lastname: Fujimoto
mesh_terms: D052242:Adiponectin / Q000097:blood* / Q000235:genetics / Q000378:metabolism; D000818:Animals; D004041:Dietary Fats / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome; D023421:Models, Animal; D010288:Parenteral Nutrition / Q000009:adverse effects*; D047492:Peroxisome Proliferator-Activated Receptors / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D054419:Receptors, Adiponectin / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D004041:Dietary Fats; D015850:Interleukin-6; D047492:Peroxisome Proliferator-Activated Receptors; D012333:RNA, Messenger; D054419:Receptors, Adiponectin; D014409:Tumor Necrosis Factor-alpha; C504339:adiponectin receptor 1, rat; D006003:Glycogen