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Effects of enteral carbohydrates on de novo lipogenesis in critically ill patients^1,2,3

¹ From the Department of Nutritional Sciences, University of California, Berkeley; the Surgical Intensive Care Unit, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; and the Institute of Physiology, Lausanne University, Lausanne, Switzerland.

Background: Conversion of glucose into lipid (de novo lipogenesis; DNL) 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 evaluate the effects of carbohydrate administered as part of continuous enteral nutrition in critically ill patients.

Design: This was a prospective, open study including 25 patients nonconsecutively admitted to a medicosurgical intensive care unit. Glucose metabolism and hepatic DNL were measured in the fasting state or after 3 d of continuous isoenergetic enteral feeding providing 28%, 53%, or 75% carbohydrate.

Results: DNL increased with increasing carbohydrate intake ( ± SEM: 7.5 ± 1.2% with 28% carbohydrate, 9.2 ± 1.5% with 53% carbohydrate, 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 multiple regression analysis, DNL was correlated with carbohydrate intake, but not with body weight or plasma insulin concentrations. Endogenous glucose production, assessed with a dual-isotope technique, was not significantly different between the 3 groups of patients (13.7–15.3 µmol • kg^-1 • min^-1), indicating impaired suppression by carbohydrate feeding. Gluconeogenesis was measured with [¹³C]bicarbonate, and increased as the carbohydrate intake increased (from 2.1 ± 0.5 µmol • kg^-1 • min^-1 with 28% carbohydrate intake to 3.7 ± 0.3 µmol • kg^-1 • min^-1 with 75% carbohydrate intake, P < 0.05).

Conclusion: Carbohydrate feeding fails to suppress endogenous glucose production and gluconeogenesis, but stimulates DNL in critically ill patients.

Key Words: Glucose production • gluconeogenesis • lipogenesis • insulin resistance • enteral nutrition • critically ill patients • de novo lipogenesis

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