Intestinal adaptation occurs independently of parenteral long-chain triacylglycerol and with no change in intestinal eicosanoids after mid-small bowel resection in rats.
The role of enteral or parenteral long-chain triacylglycerol (LCT) in the complex process of intestinal adaptation is poorly defined and may involve alterations in eicosanoid synthesis. Our objective was to determine whether provision of parenteral LCT stimulates eicosanoid synthesis and resection-induced intestinal adaptation. We assessed small bowel structural adaptation, the fatty acid profiles of liver, plasma and jejunal mucosa, and the profile of 11 eicosanoids derived from (n-6) PUFA of the jejunal mucosa in rats maintained with total parenteral nutrition (TPN) with 0 or 32% of nonprotein energy from Intralipid for 7 d after mid-small bowel resection or transection control surgery. There was no evidence of biochemical essential fatty acid (EFA) deficiency in the absence of parenteral fat. Resection-induced gut growth occurred independently of parenteral LCT based on significant mucosal hyperplasia in the jejunum and ileum. The mucosal profile of linoleic acid in the total lipid extract of jejunum increased with the presence of parenteral LCT, but decreased with resection without differences in arachidonic acid. There were no differences in the jejunal profile of 11 (n-6)-derived eicosanoids among the four TPN groups as determined by tandem MS. In summary, small bowel resection-induced adaptation occurs independently of parenteral LCT, and fat-free TPN without EFA deficiency does not alter the profile of jejunal (n-6)-derived eicosanoids. Thus, parenteral administration of LCT does not appear to alter jejunal eicosanoid synthesis nor is it beneficial in stimulating intestinal adaptation.
Dahly
Elizabeth M
EM
Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, WI 53706, USA.
Grahn
Michael J
MJ
Draxler
Angela K
AK
Ney
Denise M
DM
D000222:Adaptation, Physiological; D004041:Dietary Fats / Q000008:administration & dosage; D015237:Dinoprost / Q000032:analysis; D015232:Dinoprostone / Q000032:analysis; D015777:Eicosanoids / Q000032:analysis*; D005227:Fatty Acids / Q000008:administration & dosage / Q000032:analysis / Q000097:blood; D006965:Hyperplasia; D007082:Ileum / Q000737:chemistry / Q000473:pathology; D007413:Intestinal Mucosa / Q000737:chemistry / Q000473:pathology; D007421:Intestine, Small / Q000737:chemistry / Q000601:surgery*; D007422:Intestines / Q000502:physiology*; D007583:Jejunum / Q000737:chemistry / Q000473:pathology; D019787:Linoleic Acid / Q000008:administration & dosage / Q000097:blood; D008055:Lipids / Q000032:analysis; D008099:Liver / Q000737:chemistry; D019301:Oleic Acid / Q000032:analysis; D019308:Palmitic Acid / Q000032:analysis; D010289:Parenteral Nutrition, Total; D014280:Triglycerides / Q000008:administration & dosage*; D015430:Weight Gain
D004041:Dietary Fats; D015777:Eicosanoids; D005227:Fatty Acids; D008055:Lipids; D014280:Triglycerides; D019301:Oleic Acid; D019308:Palmitic Acid; D019787:Linoleic Acid; D015237:Dinoprost; D015232:Dinoprostone