Y. Nakai et al., Plasma concentrations of tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptors in patients with bulimia nervosa, CLIN ENDOCR, 53(3), 2000, pp. 383-388
BACKGROUND Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with numer
ous immunological and metabolic activities. In addition, TNF-alpha can stim
ulate a variety of physiological, neuroendocrine and behavioural responses
of the central nervous system. In experimental animals, TNF-alpha induces c
hanges in physiological and behavioural parameters which have also been obs
erved in eating disorders. The biological activities of TNF-alpha are media
ted by two structurally related, but functionally distinct receptors, TNF-R
I and TNF-RH. Since injection of TNF-alpha results in increased shedding of
TNF-alpha receptors, it is likely that TNF-alpha release is reflected by s
oluble TNF-receptors (sTNF-Rs) levels.
AIMS We studied plasma concentrations of TNF-alpha 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-alpha concentrations were measured by enzyme immuno
assay kit and plasma concentrations of sTNF-RI and sTNF-RII were measured b
y enzyme-linked immunosorbent assay. RESULTS Plasma TNF-alpha concentration
s 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 conc
entrations 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-alpha concentrations w
ere 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 patien
ts. However, plasma TNF-alpha concentrations were not related to body fat m
ass or to bulimic behaviours in these patients.
CONCLUSIONS Our present findings suggest that the adipose tissue may not be
the immediate source of TNF-alpha in bulimic patients but the increase in
plasma TNF-alpha in these patients may be derived from the central nervous
system sources. The elevated sTNF-RII may reflect different shedding kineti
cs compared with sTNF-RI in bulimic patients.