title: Continuous parenteral and enteral nutrition induces metabolic dysfunction in neonatal pigs.
abstract: BACKGROUND
  We previously showed that parenteral nutrition (PN) compared with formula feeding results in hepatic insulin resistance and steatosis in neonatal pigs. The current aim was to test whether the route of feeding (intravenous [IV] vs enteral) rather than other feeding modalities (diet, pattern) had contributed to the outcome.
  
  
  METHODS
  Neonatal pigs were fed enterally or parenterally for 14 days with 1 of 4 feeding modalities as follows: (1) enteral polymeric formula intermittently (FORM), (2) enteral elemental diet (ED) intermittently (IEN), (3) enteral ED continuously (CEN), and (4) parenteral ED continuously (PN). Subgroups of pigs underwent IV glucose tolerance tests (IVGTT) and hyperinsulinemic-euglycemic clamps (CLAMP). Following CLAMP, pigs were euthanized and tissues collected for further analysis.
  
  
  RESULTS
  Insulin secretion during IVGTT was significantly higher and glucose infusion rates during CLAMP were lower in CEN and PN than in FORM and IEN. Endogenous glucose production rate was suppressed to zero in all groups during CLAMP. In the fed state, plasma glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide (GLP)-1, and GLP-2 were different between feeding modalities. Insulin receptor phosphorylation in liver and muscle was decreased in IEN, CEN, and PN compared with FORM. Liver weight was highest in PN. Steatosis and myeloperoxidase (MPO) activity tended to be highest in PN and CEN. Enterally fed groups had higher plasma GLP-2 and jejunum weight compared with PN.
  
  
  CONCLUSIONS
  PN and enteral nutrition (EN) when given continuously as an elemental diet reduces insulin sensitivity and the secretion of key gut incretins. The intermittent vs continuous pattern of EN produced the optimal effect on metabolic function.
authors.affiliation: USDA/ARS Children's Nutrition Research Center, Houston, Texas 77030, USA. bstoll@bcm.edu
authors.forename: Barbara
authors.initials: B
authors.lastname: Stoll
authors.forename: Patrycja Jolanta
authors.initials: PJ
authors.lastname: Puiman
authors.forename: Liwei
authors.initials: L
authors.lastname: Cui
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Chang
authors.forename: Nancy Marie
authors.initials: NM
authors.lastname: Benight
authors.forename: Caroline
authors.initials: C
authors.lastname: Bauchart-Thevret
authors.forename: Bolette
authors.initials: B
authors.lastname: Hartmann
authors.forename: Jens Juul
authors.initials: JJ
authors.lastname: Holst
authors.forename: Douglas Guy
authors.initials: DG
authors.lastname: Burrin
mesh_terms: D061605:Administration, Intravenous; D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose / Q000032:analysis; D023381:Endpoint Determination; D004750:Enteral Nutrition / Q000009:adverse effects / Q000379:methods*; D005234:Fatty Liver / Q000503:physiopathology; D005260:Female; D005526:Food, Formulated; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism; D053767:Glucagon-Like Peptide 2 / Q000378:metabolism; D054795:Incretins / Q000378:metabolism; D007249:Inflammation / Q000503:physiopathology; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D007421:Intestine, Small / Q000187:drug effects / Q000254:growth & development; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008659:Metabolic Diseases / Q000209:etiology* / Q000503:physiopathology; D017711:Nonlinear Dynamics; D009929:Organ Size / Q000187:drug effects; D010288:Parenteral Nutrition / Q000009:adverse effects / Q000379:methods*; D013552:Swine
chemical_list: D001786:Blood Glucose; D053767:Glucagon-Like Peptide 2; D054795:Incretins; D007328:Insulin; D052216:Glucagon-Like Peptide 1