Parenteral nutrition with lipid or glucose suppresses liver growth and response to GH in adolescent male rats

Citation
A. Sevette et al., Parenteral nutrition with lipid or glucose suppresses liver growth and response to GH in adolescent male rats, AM J P-ENDO, 281(5), 2001, pp. E1063-E1072
Citations number
46
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
ISSN journal
01931849 → ACNP
Volume
281
Issue
5
Year of publication
2001
Pages
E1063 - E1072
Database
ISI
SICI code
0193-1849(200111)281:5<E1063:PNWLOG>2.0.ZU;2-8
Abstract
Our aim was to investigate the effects of modifying the carbohydrate-to-lip id ratio of parenteral nutrition (PN) on body composition and the anabolic actions of insulin-like growth factor I (IGF-I) and growth hormone (GH). Ad olescent male Sprague-Dawley rats were randomized to receive 7 days of GH, IGF-I (3.5 mg.kg(-1).day(-1) for both) or placebo while receiving high-carb ohydrate PN (CHO-PN), high-lipid PN (L-PN), or an oral diet (chow) (the PN protocols were isonitrogenous and isocaloric). PN impaired muscle growth, w hich was reversed by GH in the CHO-PN group only (P<0.03). PN increased car cass lipid (P<0.02), the effect being greater in the L-PN than in the CHO-P N group (P<0.001). Visceral lean tissue growth was significantly impaired b y PN (P<0.001). IGF-I reversed this impairment, but GH had no effect. PN im paired the normal increase in hepatic protein and DNA (P<0.001) and produce d liver steatosis (P<0.001). However, this steatosis was less in L-PN than in CHO-PN (P<0.001). Serum IGF-I and the acid-labile subunit (ALS) were dec reased by PN (P<0.001) and were not affected by GH during PN treatment. How ever, GH significantly increased serum ALS concentrations in the chow-fed r ats (P=0.032). In conclusion, modifying the CHO-to-L ratio of PN had no sig nificant effect on IGF-I action, but CHO-PN increased the peripheral effect of GH. L-PN increased carcass lipid significantly and decreased hepatic st eatosis. Nevertheless, PN caused significant liver steatosis and profound i mpairment of hepatic cell growth, which was associated with relative hepati c GH resistance.