Factors modulating food intake and energy expenditure prior to liver transplantation
DOI:
https://doi.org/10.23938/1137-6627/2016000100012Keywords:
cirrosis hepática, leptina, ghrelina, glucagón, IGF-IAbstract
ABSTRACT
Background. There is a high prevalence of nutritional disorders in patients with liver cirrhosis (LC). This study was designed to assess the relationships between liver function, IFG-I/IGFBP-3, nutritional status, leptin, ghrelin and glucagon in 21 patients waiting for liver transplantation (LT).
Methods. We studied 21 men aged 56+2.1 years who were on the LT list. They were classified according to Child-Pugh (CP) score from low to high liver dysfunction in CPA (n=4), CPB (n=11) and CPC (n=6). Body mass index (BMI) was calculated and body fat (%) was measured by air-displacement plethysmography. Resting energy expenditure (REE) and its variation over Harris-Benedict values (GER%) was assessed by indirect calorimetry. Fasting serum samples were taken to measure albumin, glucose, insulin, HbA1c, leptin, total ghrelin, glucagon, IGF-I and IGFBP3.
Results. There were no differences in fat % and leptin values in the three groups according to CP classification. The CPC group showed higher ghrelin values than CPA and CPB (p<0.05). All groups displayed high glucagon levels and GER% values superior to 100%. Positive correlations were found between glucagon and GER% (r=0.56; p<0.01) and between glucagon and ghrelin values (r=0.66; p<0.01). IGF-I and IGFBP3 were low in all groups and showed a positive correlation with plasma albumin (r=0.52; p<0.05 and r=0.45; p<0.05 respectively).
Conclusions. These results show an increase in ghrelin plasma values in patients with severe liver dysfunction. Hyperglucagonemia was correlated with GER%, supporting a role of glucagon in the hypermetabolic state associated to LC, raising the possibility of becoming a therapeutic target. The measurement of IGF-I/IGFBP3 represents a good marker of liver function in patients with LC.
Key words. Liver cirrhosis. Leptin. Ghrelin. Glucagon. IGF-I
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