Elevated circulating adiponectin levels in liver cirrhosis are associated with reduced liver function and altered hepatic hemodynamics
- 1 July 2004
- journal article
- clinical trial
- Published by American Physiological Society in American Journal of Physiology-Endocrinology and Metabolism
- Vol. 287 (1) , E82-E89
- https://doi.org/10.1152/ajpendo.00494.2003
Abstract
Adiponectin is a novel adipocytokine negatively correlated with parameters of the metabolic syndrome, such as body mass index (BMI), body fat mass (BFM), and circulating insulin levels. Furthermore, metabolic actions directly on the liver have been described. The aim of the present study was to characterize circulating adiponectin levels, hepatic turnover, and the association of adiponectin with key parameters of hepatic as well as systemic metabolism in cirrhosis, a catabolic disease. Circulating adiponectin levels and hepatic turnover were investigated in 20 patients with advanced cirrhosis. Hepatic hemodynamics [portal pressure, liver blood flow, hepatic vascular resistance, indocyanine green (ICG) half-life], body composition, resting energy expenditure, hepatic free fatty acids (FFA) and glucose turnover, and circulating levels of hormones (catecholamines, insulin, glucagon) and proinflammatory cytokines (IL-1β, TNF-α, IL-6) were also assessed. Circulating adiponectin increased dependently on the clinical stage in cirrhosis compared with controls (15.2 ± 1.7 vs. 8.2 ± 1.1 μg/ml, respectively, P < 0.01), whereas hepatic extraction decreased. Adiponectin was negatively correlated with parameters of hepatic protein synthesis (prothrombin time: r = −0.62, P = 0.003; albumin: r = −0.72, P < 0.001) but not with transaminases or parameters of lipid metabolism. In addition, circulating adiponectin increased with portal pressure (r = 0.67, P = 0.003), hepatic vascular resistance (r = 0.60, P = 0.008), and effective hepatic blood flow (ICG half-life: r = 0.69, P = 0.001). Adiponectin in cirrhosis was not correlated with BMI, BFM, parameters of energy metabolism, insulin levels, hepatic FFA and glucose turnover, and circulating proinflammatory cytokines. These results demonstrate that 1) adiponectin plasma levels in cirrhosis are significantly elevated, 2) the liver is a major source of adiponectin extraction, and 3) adiponectin levels in cirrhosis do not correlate with parameters of body composition or metabolism but exclusively with reduced liver function and altered hepatic hemodynamics.Keywords
This publication has 50 references indexed in Scilit:
- Cloning of adiponectin receptors that mediate antidiabetic metabolic effectsNature, 2003
- Disruption of Adiponectin Causes Insulin Resistance and Neointimal FormationJournal of Biological Chemistry, 2002
- Hormonal Regulation of Adiponectin Gene Expression in 3T3-L1 AdipocytesBiochemical and Biophysical Research Communications, 2002
- Adiponectin gene expression is inhibited by β‐adrenergic stimulation via protein kinase A in 3T3‐L1 adipocytesFEBS Letters, 2001
- Change in Expression of GBP28/Adiponectin in Carbon Tetrachloride-Administrated Mouse LiverBiochemical and Biophysical Research Communications, 2001
- cDNA Cloning and Expression of a Novel Adipose Specific Collagen-like Factor, apM1 (AdiposeMost Abundant Gene Transcript 1)Biochemical and Biophysical Research Communications, 1996
- Glucose Intolerance in Liver Cirrhosis: Role of Hepatic and Non-Hepatic Influencescclm, 1994
- Glucose and insulin metabolism in cirrhosisJournal of Hepatology, 1989
- Comparison of bolus and infusion methods for estimating hepatic blood flow in patients with liver disease using indocyanine greenJournal of Hepatology, 1987
- Transection of the oesophagus for bleeding oesophageal varicesBritish Journal of Surgery, 1973