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Effect of enteral feeding on hepatic steatosis induced by total parenteral nutrition


, : Effect of enteral feeding on hepatic steatosis induced by total parenteral nutrition. Jpen. Journal of Parenteral and Enteral Nutrition 18(1): 20-25

This study was designed to test the hypothesis that deprivation of enteral feeding contributes to the development of total parenteral nutrition (TPN)-induced hepatic dysfunction and that alterations of gut hormones are involved in its pathogenesis. Twenty-one adult Sprague-Dawley rats were randomized into three groups: group 1 received chow feeding ad libitum (288 kcal/kg per day); group 2 received dextrose-based TPN (320 +- 5 kcal/kg per day); and group 3 received TPN (315 +- 15 kcal/kg per day) plus chow feeding ad libitum (74 +- 1 kcal/kg per day). After 7 days, portal blood was assayed for insulin, glucagon, gastrin, peptide YY, secretin, and vasoactive intestinal polypeptide; systemic blood for determination of liver function tests and serum lipid analysis. Liver biopsies were taken for histology and staining for fat, and the remainder of the livers were removed for tissue lipid analysis. TPN induced striking hepatic steatosis with prominent histologic changes and accumulation of lipids, mainly triglycerides and cholesterol ester, in the liver. Addition of enteral feeding to TPN-treated animals significantly reduced the histologic changes as well as lipid accumulation in the liver. Portal plasma levels of gastrin and peptide YY were reduced in animals maintained on TPN alone, with no change in secretin or vasoactive intestinal polypeptide levels. Enteral supplementation increased peptide YY levels in group 3, but not to normal, while gastrin secretion remained decreased. The serum triglyceride levels were decreased in both TPN groups; no differences were detected in the serum cholesterol levels or liver function tests. Various mechanisms seem to be responsible for hepatic steatosis, some of which may in part involve a direct or an indirect action upon the liver via alterations in gastrin and peptide YY secretion.

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Accession: 002355378

PMID: 8164298

DOI: 10.1177/014860719401800120

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