肠内碳水化合物对危重症患者从头脂肪生成的影响。

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

作者信息

Schwarz J M, Chioléro R, Revelly J P, Cayeux C, Schneiter P, Jéquier E, Chen T, Tappy L

机构信息

Department of Nutritional Sciences, University of California, Berkeley.

出版信息

Am J Clin Nutr. 2000 Oct;72(4):940-5. doi: 10.1093/ajcn/72.4.940.

DOI:10.1093/ajcn/72.4.940

PMID:11010935

Abstract

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 (f1.gif" BORDER="0"> +/- 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 micromol * kg(-1) * min(-1)), indicating impaired suppression by carbohydrate feeding. Gluconeogenesis was measured with [(13)C]bicarbonate, and increased as the carbohydrate intake increased (from 2.1 +/- 0.5 micromol * kg(-1) * min(-1) with 28% carbohydrate intake to 3.7 +/- 0.3 micromol * 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.

摘要

背景

葡萄糖转化为脂质（从头脂肪生成；DNL）是营养支持期间给予的碳水化合物可能的归宿。如果不超过脂质氧化，它无法通过间接测热法等传统方法检测到。

目的

评估作为持续肠内营养一部分给予的碳水化合物对重症患者的影响。

设计

这是一项前瞻性、开放性研究，纳入了25例非连续入住内科-外科重症监护病房的患者。在空腹状态下或连续等能量肠内喂养3天后测量葡萄糖代谢和肝脏DNL，肠内喂养提供28%、53%或75%的碳水化合物。

结果

DNL随着碳水化合物摄入量的增加而增加（平均值±标准误：28%碳水化合物时为7.5±1.2%，53%碳水化合物时为9.2±1.5%，75%碳水化合物时为19.4±3.8%），而在一组平均禁食28小时的患者中几乎为零（1.0±0.2%）。在多元回归分析中，DNL与碳水化合物摄入量相关，但与体重或血浆胰岛素浓度无关。用双同位素技术评估的内源性葡萄糖生成在3组患者之间无显著差异（13.7 - 15.3微摩尔·千克⁻¹·分钟⁻¹），表明碳水化合物喂养对其抑制作用受损。用[¹³C]碳酸氢盐测量糖异生，其随着碳水化合物摄入量的增加而增加（碳水化合物摄入量为28%时为2.1±0.5微摩尔·千克⁻¹·分钟⁻¹，碳水化合物摄入量为75%时为3.7±0.3微摩尔·千克⁻¹·分钟⁻¹，P < 0.05）。