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Morning Preprandial Plasma Ghrelin and Catecholamine Concentrations in Patients with Phenylketonuria and Normal Controls: Evidence for Catecholamine-Mediated Ghrelin Regulation

Institute of Child Health (K.H.S.), 11527 Athens, Greece; Department of Clinical Biochemistry, Aghia Sophia Children’s Hospital (I.P., M.V., G.A.K.), 11527 Athens, Greece; Blood Transfusion Service, Henri Dunant Hospital (M.V.), 11527 Athens, Greece; and Departments of Experimental Physiology (S.T.) and Pediatrics (G.P.C.), Athens University Medical School, 11527 Athens, Greece

Address all correspondence and requests for reprints to: Dr. I. Papassotiriou, Department of Clinical Biochemistry, Aghia Sophia Children’s Hospital, 11527 Athens, Greece. E-mail: biochem{at}paidon-agiasofia.gr.

Patients with phenylketonuria (PKU) have a diet-controlled deficiency in the conversion of phenylalanine (Phe) to tyrosine (Tyr), leading to decreased production of noradrenaline, adrenaline, and dopamine. Poor diet control results in high plasma Phe and low plasma Tyr and catecholamine concentrations. Ghrelin, a recently described gastrointestinal hormone that is elevated in the fasting state and low in the fed state, is considered a major appetite-stimulating hormone, possibly involved in the generation of obesity and insulin resistance. We evaluated morning preprandial plasma ghrelin levels in 14 diet-controlled and 15 poorly controlled PKU patients and 20 age- and body mass index (BMI)-matched healthy children (controls) and correlated its concentrations with those of Phe and catecholamines as well as with their BMI and 24-h nutrient intake. Plasma ghrelin levels were measured by RIA, plasma catecholamine concentrations were determined by HPLC with electrochemical detection, and Phe and Tyr levels were measured in an amino acid analyzer. The ghrelin concentration (744 ± 25 ng/liter) in diet-controlled patients did not differ from that in controls (802 ± 26 ng/liter; P > 0.05). On the contrary, the ghrelin concentration was significantly reduced in poorly controlled patients (353 ± 23 ng/liter; P < 0.0001). Ghrelin correlated negatively with Phe in all three groups, whereas it correlated positively with catecholamine levels and energy intake and negatively with BMI only in diet-controlled patients and controls. We conclude that ghrelin secretion may receive positive direct or indirect input from catecholamines. The absence of a correlation between ghrelin and catecholamines, energy intake, or BMI in PKU patients on an inadequate diet may be due to dysregulation of their neuroendocrine system and might be affected by high Phe levels in the stomach and/or central nervous system.

Abbreviations: A, Adrenaline; BMI, body mass index; CV, coefficient of variation; DA, dopamine; NA, noradrenaline; Phe, phenylalanine; PKU, phenylketonuria; Tyr, tyrosine.

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