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肝硬化中碳水化合物诱导的产热:葡萄糖与果糖

Carbohydrate-induced thermogenesis in liver cirrhosis: glucose vs. fructose.

作者信息

Martines D, Martines V, Pasini M, Cocco G, Lora L, Varnier M, Venier G B, Sammartano G, Naccarato R

机构信息

Department of Gastroenterology, University of Padua, Italy.

出版信息

Nutrition. 1994 Nov-Dec;10(6):521-6.

PMID:7703598
Abstract

Reduced thermic response after a glucose load has been reported in liver cirrhosis. To determine the mechanism and the site of this phenomenon, the effects of glucose and fructose on energy expenditure (EE) were measured in seven well-nourished cirrhotic patients and in six healthy control subjects. EE and fuel utilization were measured via indirect calorimetry for 3 h after oral glucose or fructose administration (1 g/kg body wt). After a glucose load, plasma glucose and insulin concentrations were higher in cirrhotic patients than in control subjects (p < 0.05). During the glucose trial, the cumulative incremental changes in EE over the 3-h measurement period were lower (p < 0.01) in patients than in the control subjects (0.98 +/- 0.13 vs. 1.70 +/- 0.23 kJ.kg-1.3 h-1). After fructose ingestion, the cumulative changes in the EE of control subjects (1.76 +/- 0.24 kJ.kg-1.3 h-1) and cirrhotic patients (1.59 +/- 0.15 kJ.kg-1.3 h-1) were similar. In cirrhotic patients, the EE increase after fructose was higher than after glucose (p < 0.05). After glucose and fructose ingestion, no difference was observed between the carbohydrate oxidation in cirrhotic patients and that in control subjects, and lipid oxidation was suppressed to the same extent in both groups. We conclude that glucose-induced thermogenesis is impaired in liver cirrhosis, whereas fructose can normalize the thermic response. Because fructose is chiefly metabolized in the liver, these findings suggest that extrahepatic tissues are the site of defective thermogenesis in liver cirrhosis.

摘要

据报道,肝硬化患者葡萄糖负荷后热反应降低。为了确定这一现象的机制和部位,在7名营养良好的肝硬化患者和6名健康对照者中测量了葡萄糖和果糖对能量消耗(EE)的影响。口服葡萄糖或果糖(1 g/kg体重)后,通过间接测热法测量3小时的EE和燃料利用情况。葡萄糖负荷后,肝硬化患者的血浆葡萄糖和胰岛素浓度高于对照者(p<0.05)。在葡萄糖试验期间,患者在3小时测量期内EE的累积增量变化低于对照者(p<0.01)(0.98±0.13 vs.1.70±0.23 kJ·kg-1·3 h-1)。果糖摄入后,对照者(1.76±0.24 kJ·kg-1·3 h-1)和肝硬化患者(1.59±0.15 kJ·kg-1·3 h-1)的EE累积变化相似。在肝硬化患者中,果糖后EE的增加高于葡萄糖后(p<0.05)。葡萄糖和果糖摄入后,肝硬化患者与对照者的碳水化合物氧化无差异,两组脂质氧化均受到同等程度的抑制。我们得出结论,肝硬化患者葡萄糖诱导的产热受损,而果糖可使热反应正常化。由于果糖主要在肝脏中代谢,这些发现表明肝外组织是肝硬化中产热缺陷的部位。

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