GLUCONEOGENESIS IN CIRRHOSIS

本研究的目的是：1)测量全身总葡萄糖输出量 和糖异生在肝硬变患者中的变化及间接评估 禁食时的糖原分解；2)评价 糖异生和间接的糖原分解作用 外源性胰升糖素抑制内源性胰岛素和胰升糖素 通过输注生长抑素；3)测定蛋白水解率 以及禁食期间的蛋白质氧化和尿素合成；以及4) 量化总能量消耗和氧化底物的类型 肝硬变患者禁食期间与年龄/性别匹配的对照组之间的关系 他们的肝脏大小。假设是：1)为了维持 肝硬变患者的基础葡萄糖产生、糖异生是 增加；2)血浆胰高血糖素水平升高是导致这种情况的原因 糖异生增加；以及3)糖异生增加 糖异生是通过增加肌肉蛋白分解和蛋白质来维持的 氧化会导致肌肉蛋白质的浪费。A初步数据 在前2名患者和2名对照受试者之后进行分析 ，并对其进行了研究。在糖异生方面，我们没有区别 假设是24小时葡萄糖输注掩盖了 两组间差异有统计学意义。已修改协议以添加一个测试 没有葡萄糖负荷的一天。所获得的生物样本是 目前正在分析中。

The aims of this study are: 1) to measure total systemic glucose output and gluconeogenesis in patients with cirrhosis and indirectly estimate glycogenolysis during fasting; 2) to evaluate the sensitivity of gluconeogenesis and, indirectly, glycogenolysis, to the action of exogenous glucagon while endogenous insulin and glucagon are suppressed by an infusion of somatostatin; 3) to measure the rate of proteolysis and protein oxidation and urea synthesis during fasting; and 4) to quantify total energy expenditure and the type of substrates oxidized during fasting in cirrhotics and age/sex matched controls and to relate them to the liver size. The hypotheses are: 1) in order to maintain basal glucose production, gluconeogenesis in cirrhotic patients is increased; 2) elevated plasma glucagon levels contribute to this increase in gluconeogenesis; and 3) the increased rate of gluconeogenesis is sustained by increased muscle proteolysis and protein oxidation leading to muscle protein wasting. A preliminary data analysis was conducted after the first 2 patients and 2 control subjects were studied. There was no difference in gluconeogenesis which we hypothesize is the result of the 24hr glucose infusion masking any differences in the two groups. The protocol was modified to add a test day without glucose loading. the biological samples obtained are currently being analyzed.