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Department of Nutritional Sciences, University of Wisconsin-Madison, WI 53706;
* Department of Biochemistry, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229; and
Departments of Statistics and Plant Pathology, University of Wisconsin-Madison, Madison, WI 53706
2To whom correspondence should be addressed. E-mail: ney{at}nutrisci.wisc.edu.
The optimal level of energy for critically ill patients who require parenteral nutrition (PN) is unclear. Our objective was to determine whether 50% energy (50%E) restriction due to a reduction in carbohydrate or fat, with provision of adequate protein and micronutrients, ameliorates the detrimental effects of dexamethasone (Dex) on body protein catabolism, insulin resistance, and insulin-like growth factor-I (IGF-I) responses in rats administered PN. The experiment included 6 PN groups, adequate energy (AE) ± Dex, 50% AE with high carbohydrate (50%E
CHO) ± Dex and 50% AE with high fat (50%E
FAT) ± Dex. There was a significant interaction between energy level and Dex such that the increase in body catabolism due to 50%E from
CHO or
FAT was reduced by
50%, although the amount of body weight and nitrogen lost over 7 d was significantly greater with 50%E than with AE. AE+Dex induced a 60% increase in liver mass, whereas 50%E+Dex reduced the increase to 26%. AE+Dex induced a 5-fold increase in serum insulin level, whereas 50%E+Dex normalized the insulin to glucose ratio. Serum IGF-I levels were reduced 1418% by Dex and 30% by 50%E. Hepatic immunoreactive IGF-I was significantly correlated with serum IGF-I and nitrogen balance. 50%E
CHO and 50%E
FAT had differential effects on hepatic IGF-I mRNA with a 40% decrease in IGF-I mRNA due to 50%E
FAT+Dex. In summary,
CHO or
FAT hypoenergetic PN with adequate protein had similar effects in normalizing hyperinsulinemia, attenuating hepatomegaly, and reducing the increment, but not the total amount of body protein catabolism, induced by glucocorticoid excess.
KEY WORDS: glucocorticoids insulin nitrogen catabolism insulin-like growth factor-I
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