GLUCONEOGENESIS IN CIRRHOSIS

本研究的目的是：1）测量全身葡萄糖输出量 肝硬化患者的肝硬化发生率，并间接评估 空腹时糖原分解; 2）评估 糖原分解的作用， 外源性胰高血糖素，而内源性胰岛素和胰高血糖素被抑制 通过输注生长抑素; 3）测量蛋白水解速率 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 在禁食期间，在糖尿病患者和年龄/性别匹配的对照中， 肝脏的大小。 假设是：1）为了维持 基础葡萄糖生成，糖尿病患者的胰岛素生成， 增加; 2）升高的血浆胰高血糖素水平有助于这一点 （3）增加了新生儿的出生率; 通过增加肌肉蛋白水解和蛋白质合成来维持骨骼肌再生 氧化导致肌肉蛋白质消耗。 的初步数据 在前2名患者和2名对照受试者 研究了 我们发现， 假设是24小时葡萄糖输注掩盖了任何 两组的差异。 对方案进行了修改，以增加一项测试 无葡萄糖负荷的一天。 所获得的生物样品是 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.