Müller M J, Rieger A, Willmann O, Lautz H U, Balks H J, Von Zur Mühlen A, Canzler H, Schmidt F W
Medizinische Hochschule Hannover, Department Innere Medizin, Gastroenterologie und Hepatologie und Klinische Endokrinologie, Konstanty-Gutschow-Str. 8, D 3000, Hannover 61, Germany.
Clin Nutr. 1992 Aug;11(4):193-206. doi: 10.1016/0261-5614(92)90028-o.
Energy expenditure, whole body substrate oxidation rates and arterial substrate concentrations were measured in 14 patients with liver cirrhosis and 13 control subjects before and during sequential infusions of a long chain (LCT) or a medium chain triglyceride emulsion (MCT) without and with concomitant insulin plus glucose infusions. Resting energy expenditure, basal substrate oxidation rates and the arterial concentrations of glucose, lactate, triglycerides and ketones were normal, whereas plasma free fatty acids and glycerol were both increased in patients with liver cirrhosis. The arterial plasma triglyceride and free fatty acid concentrations as well as whole body lipid oxidation rate rose in response to LCT in both groups and the maximum lipid oxidation rate was 1.1 or 1.3 mg/kg fat free mass x min in controls and in cirrhotics, respectively (n.s.). Concomitantly, glucose oxidation rate fell to 65% of basal values in controls (p < 0.01), but remained nearly unchanged in the cirrhotic group (89% of the basal value; n.s.). The increase in plasma ketones was reduced to 67% of control values in liver cirrhosis (p < 0.01). Only a slight effect on energy expenditure was observed in both groups. When compared to controls, liver cirrhosis impaired insulin-induced increases in glucose disposal (-30%, p < 0.01) and in non oxidative glucose metabolism (-93%, p < 0.01). Concomitantly, normal increases in energy expenditure, glucose oxidation rate and the arterial plasma lactate concentrations and normal decreases in lipolysis, lipid oxidation and ketogenesis were observed in patients with liver cirrhosis. When lipids were given together with glucose, energy expenditure and lipid oxidation increased in controls, but glucose was the preferred fuel oxidised and lipid-induced thermogenesis was reduced in the cirrhotic group. Using a 50% MCT-emulsion, plasma free fatty acid concentrations further increased, but energy expenditure and lipid oxidation remained unchanged in both groups and further increases in plasma ketones were only observed in controls. Infusing glycerol in a subgroup of patients showed no thermogenic effect and a reduced glycerol clearance in liver cirrhosis.
在14例肝硬化患者和13例对照受试者中，在连续输注长链（LCT）或中链甘油三酯乳剂（MCT）之前和期间，分别在无胰岛素加葡萄糖输注以及有胰岛素加葡萄糖输注的情况下，测量了能量消耗、全身底物氧化率和动脉底物浓度。静息能量消耗、基础底物氧化率以及葡萄糖、乳酸、甘油三酯和酮的动脉浓度均正常，而肝硬化患者的血浆游离脂肪酸和甘油均升高。两组中，动脉血浆甘油三酯和游离脂肪酸浓度以及全身脂质氧化率均因LCT而升高，对照组和肝硬化组的最大脂质氧化率分别为1.1或1.3mg/kg去脂体重×分钟（无显著差异）。同时，对照组的葡萄糖氧化率降至基础值的65%（p<0.01），但肝硬化组几乎保持不变（基础值的89%；无显著差异）。肝硬化患者血浆酮的增加降至对照组值的67%（p<0.01）。两组中仅观察到对能量消耗有轻微影响。与对照组相比，肝硬化损害了胰岛素诱导的葡萄糖处置增加（-30%，p<0.01）和非氧化葡萄糖代谢增加（-93%，p<0.01）。同时，肝硬化患者观察到能量消耗、葡萄糖氧化率和动脉血浆乳酸浓度正常增加，脂解、脂质氧化和生酮作用正常降低。当脂质与葡萄糖一起给予时，对照组的能量消耗和脂质氧化增加，但肝硬化组中葡萄糖是首选的氧化燃料，脂质诱导的产热减少。使用50%的MCT乳剂时，血浆游离脂肪酸浓度进一步升高，但两组的能量消耗和脂质氧化均保持不变，仅在对照组中观察到血浆酮进一步增加。在一组患者中输注甘油未显示产热作用，且肝硬化患者的甘油清除率降低。
