Kalaitzakis Evangelos, Bosaeus Ingvar, Ohman Lena, Björnsson Einar
Department of Internal Medicine, Faculty of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
Am J Clin Nutr. 2007 Mar;85(3):808-15. doi: 10.1093/ajcn/85.3.808.
Liver cirrhosis is associated with reduced energy intake and increased resting energy expenditure.
We aimed to investigate the possible role of glucose, insulin, leptin, and ghrelin in the pathogenesis of these alterations.
Nutritional status, energy intake, resting energy expenditure, and fasting glucose, insulin, and leptin were assessed in 31 patients with cirrhosis. Postprandial glucose, insulin, C-peptide, leptin, and ghrelin responses were studied in a subgroup of patients after a standard meal. Ten healthy subjects served as controls.
Patients with cirrhosis had a lower energy intake (P < 0.05), higher resting energy expenditure (P < 0.05), higher fasting leptin (P < 0.05), and higher insulin resistance (P < 0.001) than did the healthy control subjects. In the patients with cirrhosis, fasting leptin was negatively correlated with resting energy expenditure (r = -0.38, P < 0.05) but not with energy intake. In control subjects, leptin was negatively correlated with energy intake (r = -0.72, P < 0.05) but not with resting energy expenditure. The patients with cirrhosis had higher postprandial glucose (P < 0.001) and lower ghrelin (P < 0.05) concentrations at 4 h postprandially than did the control subjects. The increase in ghrelin from its minimal postmeal value to 4 h postmeal was negatively correlated (r = -0.66, P = 0.014) with weight loss in the patients with cirrhosis. Energy intake was negatively correlated (r = -0.42, P < 0.01) with the postprandial increase in glucose.
In cirrhosis, altered postprandial glucose and ghrelin are associated with reduced energy intake and weight loss, respectively, and the effects of leptin on energy intake and expenditure seem to be altered. Insulin resistance might be involved in these altered postprandial responses.
肝硬化与能量摄入减少及静息能量消耗增加有关。
我们旨在研究葡萄糖、胰岛素、瘦素和胃饥饿素在这些改变的发病机制中可能发挥的作用。
对31例肝硬化患者的营养状况、能量摄入、静息能量消耗以及空腹血糖、胰岛素和瘦素进行评估。在一个亚组患者进食标准餐后，研究其餐后血糖、胰岛素、C肽、瘦素和胃饥饿素的反应。10名健康受试者作为对照。
与健康对照受试者相比，肝硬化患者的能量摄入较低（P < 0.05），静息能量消耗较高（P < 0.05），空腹瘦素较高（P < 0.05），胰岛素抵抗较高（P < 0.001）。在肝硬化患者中，空腹瘦素与静息能量消耗呈负相关（r = -0.38，P < 0.05），但与能量摄入无关。在对照受试者中，瘦素与能量摄入呈负相关（r = -0.72，P < 0.05），但与静息能量消耗无关。肝硬化患者餐后4小时的餐后血糖较高（P < 0.001），胃饥饿素浓度较低（P < 0.05）。肝硬化患者胃饥饿素从餐后最低值到餐后4小时的增加与体重减轻呈负相关（r = -0.66，P = 0.014）。能量摄入与餐后血糖升高呈负相关（r = -0.42，P < 0.01）。
在肝硬化中，餐后葡萄糖和胃饥饿素的改变分别与能量摄入减少和体重减轻有关，并且瘦素对能量摄入和消耗的影响似乎发生了改变。胰岛素抵抗可能参与了这些餐后反应的改变。
