Effects of enteral carbohydrates on de novo lipogenesis in critically ill patients

Citation
Jm. Schwarz et al., Effects of enteral carbohydrates on de novo lipogenesis in critically ill patients, AM J CLIN N, 72(4), 2000, pp. 940-945
Citations number
27
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF CLINICAL NUTRITION
ISSN journal
00029165 → ACNP
Volume
72
Issue
4
Year of publication
2000
Pages
940 - 945
Database
ISI
SICI code
0002-9165(200010)72:4<940:EOECOD>2.0.ZU;2-H
Abstract
Background: Conversion of glucose into Lipid (de novo lipogenesis: BNL) is a possible fate of carbohydrate administered during nutritional support. It cannot be detected by conventional methods such as indirect calorimetry if it does not exceed lipid oxidation. Objective: The objective was to evalua te the effects of carbohydrate administered as part of continuous enteral n utrition in critically ill patients. Design: This was a prospective. open study including 25 patients nonconsecu tively admitted to a medicosurgical intensive care unit. Glucose metabolism and hepatic DNL, were measured in the fasting state or after 3 d of contin uous isoenergetic enteral feeding providing 28%, 53%, or 75% carbohydrate. Results: DNL increased with increasing carbohydrate intake ((x) over bar +/ - SEM: 7.5 +/- 1.28 with 28% carbohydrate, 9.2 +/- 1.5% with 53% carbohydra te, and 19.4 +/- 3.8% with 75% carbohydrate) and was nearly zero in a group of patients who had fasted for an average of 28 h (1.0 +/- 0.2%). In multi ple regression analysis, DNL was correlated with carbohydrate intake, but n ot with body weight or plasma insulin concentrations. Endogenous glucose pr oduction. assessed with a dual-isotope technique, :vas not significantly di fferent between the 3 groups of patients (13.7-15.3 mu mol.kg(-1).min(-1)), indicating impaired suppression by carbohydrate feeding. Gluconeogenesis w as measured with [C-13]bicarbonate, and increased as the carbohydrate intak e increased (from 2.1 +/- 0.5 mu mol.kg(-10).min(-1) with 28% carbohydrate intake to 3.7 +/- 0.3 mu mol.kg(-1).min(-1) with 75% carbohydrate intake, P < 0.05). Conclusion: Carbohydrate feeding fails to suppress endogenous glucose produ ction and gluconeogenesis, but stimulates DNL in critically ill patients.