Increased plasma adiponectin concentrations in poorly controlled patients with phenylketonuria normalize with a strict diet: evidence for catecholamine-mediated adiponectin regulation and a complex effect of phenylketonuria diet on atherogenesis risk factors

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3097497 19 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Increased plasma adiponectin concentrations in poorly controlled
patients with phenylketonuria normalize with a strict diet: evidence for
catecholamine-mediated adiponectin regulation and a complex effect of
phenylketonuria diet on atherogenesis risk factors
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Adiponectin (Adpn), an adipose tissue-derived hormone, prevents
endothelial inflammation and early atherogenesis. Classic
phenylketonuria (PKU), an inborn error of phenylalanine (Phe)
metabolism, results in a reduction of catecholamine biosynthesis and
requires treatment with lifelong low-Phe diet to prevent mental
dysfunction and allow proper intellectual development. In this study, we
evaluated the effect of the quality of PKU diet on plasma Adpn
concentrations and related biochemical indices of endothelial
dysfunction and atherogenesis. Patients with PKU were divided into
groups A (n = 18), who were on a strict diet, and B (n = 18), who were
on a loose diet, after evaluation of their 30-day dietetic diaries and
measurement of Phe blood concentrations. Twenty healthy children of
similar ages and body mass indexes served as controls (group C). Group A
patients had normal circulating catecholamines and Adpn and decreased
tumor necrosis factor alpha concentrations and low-density lipoprotein
cholesterol/apolipoprotein B ratio compared with groups B and C. Despite
these favorable parameters, however, homocysteine concentration was
twice as high in group A compared with groups B and C. Interestingly,
group B patients under loose dietary control had significantly elevated
Adpn concentrations compared with groups A and C and increased tumor
necrosis factor alpha and an unfavorable lipid profile, but normal
levels of hornocysteine. These data support the hypothesis that
catecholamines inhibit Adpn secretion and that the elevated Adpn of the
poorly controlled patients might moderate their risk for endothelial
dysfunction and atherogenesis. Homocysteine production appears to be
unfavorably affected by a strict PKU diet, diverging from the rest of
the atherogenesis risk factors, which were improved in the
well-controlled patients. (c) 2005 Elsevier Inc. All rights reserved.
Έτος δημοσίευσης:
2005
Συγγραφείς:
Schulpis, KH
Papassotiriou, I
Tsakiris, S
Vounatsou, M and
Chrousos, GP
Περιοδικό:
Metabolism: Clinical and Experimental
Εκδότης:
W B SAUNDERS CO-ELSEVIER INC
Τόμος:
54
Αριθμός / τεύχος:
10
Σελίδες:
1350-1355
Επίσημο URL (Εκδότης):
DOI:
10.1016/j.metabol.2005.04.025
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