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

被引:1
|
作者
Schwarz, JM
Chioléro, R
Revelly, JP
Cayeux, C
Schneiter, P
Jéquier, E
Chen, T
Tappy, L
机构
[1] Univ Lausanne, Inst Physiol, CH-1005 Lausanne, Switzerland
[2] Univ Calif Berkeley, Dept Nutr Sci, Berkeley, CA 94720 USA
[3] CHU Vaudois, Surg Intens Care Unit, CH-1011 Lausanne, Switzerland
来源
关键词
glucose production; gluconeogenesis; lipogenesis; insulin resistance; enteral nutrition; critically ill patients; de novo lipogenesis;
D O I
暂无
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
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 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 ((x) over bar +/- SEM: 7.5 +/- 1.28 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, :vas not significantly different between the 3 groups of patients (13.7-15.3 mu mol.kg(-1).min(-1)), indicating impaired suppression by carbohydrate feeding. Gluconeogenesis was measured with [C-13]bicarbonate, and increased as the carbohydrate intake 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 production and gluconeogenesis, but stimulates DNL in critically ill patients.
引用
收藏
页码:940 / 945
页数:6
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