EFFECT OF ENTERAL FEEDING ON HEPATIC STEATOSIS INDUCED BY TOTAL PARENTERAL-NUTRITION

Citation
O. Zamir et al., EFFECT OF ENTERAL FEEDING ON HEPATIC STEATOSIS INDUCED BY TOTAL PARENTERAL-NUTRITION, JPEN. Journal of parenteral and enteral nutrition, 18(1), 1994, pp. 20-25
Citations number
42
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
01486071
Volume
18
Issue
1
Year of publication
1994
Pages
20 - 25
Database
ISI
SICI code
0148-6071(1994)18:1<20:EOEFOH>2.0.ZU;2-P
Abstract
This study was designed to test the hypothesis that deprivation of ent eral feeding contributes to the development of total parenteral nutrit ion (TPN)-induced hepatic dysfunction and that alterations of gut horm ones 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 kca l/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; systemi c blood for determination of liver function tests and serum lipid anal ysis. Liver biopsies were taken for histology and staining for fat, an d the remainder of the livers were removed for tissue lipid analysis. TPN induced striking hepatic steatosis with prominent histologic chang es and accumulation of lipids, mainly triglycerides and cholesterol es ter, in the liver. Addition of enteral feeding to TPN-treated animals significantly reduced the histologic changes as well as lipid accumula tion in the liver. Portal plasma levels of gastrin and peptide YY were reduced in animals maintained on TPN alone, with no change in secreti n or vasoactive intestinal polypeptide levels. Enteral supplementation increased peptide YY levels in group 3, but not to normal, while gast rin secretion remained decreased. The serum triglyceride levels were d ecreased in both TPN groups; no differences were detected in the serum cholesterol levels or liver function tests. Various mechanisms seem t o be responsible for hepatic steatosis, some of which may in part invo lve a direct or an indirect action upon the liver via alterations in g astrin and peptide YY secretion.