Abnormal plasma peptide YY3–36 levels in patients with liver cirrhosis

ObjectivePeptide YY3–36 (PYY3–36) is a gut hormone with anorectic action that also affects energy expenditure. Anorexia and malnutrition are often observed in patients with decompensated liver cirrhosis (LC), whereas patients with LC after insertion of transjugular portosystemic stent shunts (TIPS) show normal eating behavior. The underlying mechanism of anorexia in decompensated LC and its resolution in patients with TIPS is still unclear. We thus investigated fasting and postprandial PYY3–36 serum levels in patients with decompensated LC, patients with compensated LC with in situ TIPS, and healthy controls.MethodsWe analyzed fasting PYY3–36 levels in six patients with decompensated LC (four men and two women, 55 ± 11 y of age), nine patients with TIPS (seven men and two women, 48 ± 11 y of age), and 10 controls (eight men and two women, 43 ± 9 y of age) postprandially after a standardized meal of 300 kcal and during 1-h continuous parenteral nutrition. Energy expenditure was determined by indirect calorimetry.ResultsAt baseline PYY3–36 was comparable in controls and patients with TIPS (91 ± 10 and 89 ± 25 ng/L) but was increased in patients with decompensated LC (165 ± 44 ng/L, P < 0.01). Although the cumulative postprandial PYY3–36 increase was similar in controls (mean 2089 ng/240 min per liter) and patients with decompensated LC (mean 1735 ng/240 min per liter), no postprandial PYY3–36 increase was observed in patients with TIPS (mean −579 ng/240 min per liter). Parenteral nutrition did not significantly affect PYY3–36 levels in any group. Fasting PYY3–36 values were negatively related to resting energy expenditure (r = −0.443, P = 0.030). PYY3–36 was not associated to liver parameters (e.g., bilirubin, alanine aminotransferase).ConclusionOur results demonstrate an abnormal neuroendocrine regulation of PYY3–36 in patients with decompensated LC and those with TIPS.