Nolte W, Hartmann H, Ramadori G
Department of Gastroenterology and Endocrinology, University of Göttingen, Germany.
Exp Clin Endocrinol Diabetes. 1995;103(2):63-74. doi: 10.1055/s-0029-1211331.
Chronic liver disease is characterized by numerous metabolic alterations, predominantly catabolic, resulting in the clinical picture of malnutrition and even cachexia in some patients. The following review focuses on disturbances of glucose metabolism and of hormonal interactions that could contribute to the clinical picture of malnutrition seen in chronic liver disease. Body composition is altered in a characteristic manner with an increase in fat mass and a significant loss of muscle tissue. Furthermore, defective glucose storage due to reduced insulin sensitivity predominantly of muscle tissue has been observed. The pathogenesis of insulin resistance leading to an impaired glucose tolerance or a manifest diabetes mellitus is as yet unknown. A receptor/postreceptor dysfunction probably exists in chronic liver disease that might be explained by the following factors: 1. Altered membrane lipid composition and increased levels of free fatty acids; 2. long-lasting hyperinsulinemia; 3. increased plasma levels of insulin counteracting hormones such as growth hormone, glucagon, catecholamines and possibly cytokines; 4. a lack of liver-derived humoral factors with insulin-like activity, i.e. insulin-like growth factors I and II.
慢性肝病的特征是存在众多代谢改变，主要是分解代谢，这在一些患者中导致营养不良甚至恶病质的临床表现。以下综述聚焦于葡萄糖代谢紊乱以及可能导致慢性肝病中所见营养不良临床表现的激素相互作用。身体组成以一种特征性方式改变，脂肪量增加而肌肉组织显著丢失。此外，已观察到主要由于肌肉组织胰岛素敏感性降低导致葡萄糖储存缺陷。导致糖耐量受损或明显糖尿病的胰岛素抵抗的发病机制尚不清楚。慢性肝病中可能存在受体/受体后功能障碍，这可能由以下因素解释：1. 膜脂质组成改变和游离脂肪酸水平升高；2. 长期高胰岛素血症；3. 胰岛素拮抗激素如生长激素、胰高血糖素、儿茶酚胺以及可能的细胞因子的血浆水平升高；4. 缺乏具有胰岛素样活性的肝脏来源的体液因子，即胰岛素样生长因子I和II。
