Exp Clin Endocrinol Diabetes 1995; 103(2): 63-74
DOI: 10.1055/s-0029-1211331

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Glucose metabolism and liver cirrhosis

W. Nolte, H. Hartmann, G. Ramadori
  • Department of Gastroenterology and Endocrinology, University of Göttingen, Göttingen, Germany
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Publication History

Publication Date:
15 July 2009 (online)


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.

Abbreviations: HGP=hepatic glucose production; IGF I and II = insulin-like growth factor I and II; TNF = tumor necrosis factor; IL-1 and -6 = Interleukin-1 and -6; IFN = interferon; EGF = epidermal growth factor; NIDDM = non insulin dependent diabetes mellitus; IDDM = insulin dependent diabetes mellitus; FFM = fat free mass; FM = fat mass.