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Plasma concentrations of tumor necrosis factor‐α (TNF‐α) and soluble TNF receptors in patients with bulimia nervosa
Author(s) -
Nakai Yoshikatsu,
Hamagaki Seiji,
Takagi Ryuro,
Taniguchi Ataru,
Kurimoto Fumihiko
Publication year - 2000
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.2000.01091.x
Subject(s) - tumor necrosis factor alpha , endocrinology , medicine , receptor , cytokine , bulimia nervosa , alpha (finance) , chemistry , biology , eating disorders , construct validity , nursing , psychiatry , patient satisfaction
BACKGROUND Tumor necrosis factor‐α (TNF‐α) is a cytokine with numerous immunological and metabolic activities. In addition, TNF‐α can stimulate a variety of physiological, neuroendocrine and behavioural responses of the central nervous system. In experimental animals, TNF‐α induces changes in physiological and behavioural parameters which have also been observed in eating disorders. The biological activities of TNF‐α are mediated by two structurally related, but functionally distinct receptors, TNF‐RI and TNF‐RII. Since injection of TNF‐α results in increased shedding of TNF‐α receptors, it is likely that TNF‐α release is reflected by soluble TNF‐receptors (sTNF‐Rs) levels. AIMS We studied plasma concentrations of TNF‐α and two sTNF‐Rs (sTNF‐RI and sTNF‐RII) in female patients with bulimia nervosa. DESIGN AND PATIENTS Twenty female patients with bulimia nervosa (BN) and 20 age‐matched normal women (N) were studied. MEASUREMENTS Plasma TNF‐α concentrations were measured by enzyme immunoassay kit and plasma concentrations of sTNF‐RI and sTNF‐RII were measured by enzyme‐linked immunosorbent assay. RESULTS Plasma TNF‐α concentrations in BN were significantly higher than those in N (4.7 ± 0.5 ng/l vs . 1.6 ± 0.1 ng/l; P < 0.01). Although no significant difference was observed in plasma sTNF‐RI concentrations between the two groups, plasma sTNF‐RII concentrations in BN were significantly higher than those in N (2080.0 ± 107.5 ng/l vs . 1569.5 ± 84.0 ng/l; P < 0.01). Plasma TNF‐α concentrations were significantly related to plasma sTNF‐RI concentrations ( r = 0.511, P < 0.05) and to plasma sTNF‐RII concentrations ( r = 0.532, P < 0.05) in bulimic patients. However, plasma TNF‐α concentrations were not related to body fat mass or to bulimic behaviours in these patients. CONCLUSIONS Our present findings suggest that the adipose tissue may not be the immediate source of TNF‐α in bulimic patients but the increase in plasma TNF‐α in these patients may be derived from the central nervous system sources. The elevated sTNF‐RII may reflect different shedding kinetics compared with sTNF‐RI in bulimic patients.