Cytokine production in patients with anorexia nervosa, bulimia nervosa, and obesity
Objective We previously reported elevated serum levels of the cytokines interleukin‐6 (IL‐6) and transforming growth factor‐β (TGF‐β) in patients with anorexia nervosa (AN). We investigated the cellular production of these two cytokines and of interferon‐γ (IFN‐γ), interleukin‐1α (IL‐1α), and tumor...
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Veröffentlicht in: | The International journal of eating disorders 2000-11, Vol.28 (3), p.293-302 |
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Sprache: | eng |
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Zusammenfassung: | Objective
We previously reported elevated serum levels of the cytokines interleukin‐6 (IL‐6) and transforming growth factor‐β (TGF‐β) in patients with anorexia nervosa (AN). We investigated the cellular production of these two cytokines and of interferon‐γ (IFN‐γ), interleukin‐1α (IL‐1α), and tumor necrosis factor‐α (TNF‐α) in subjects with AN, bulimia nervosa (BN), and obesity as well as in normal‐weight control subjects.
Methods
Supernatant fluids from isolated peripheral blood mononuclear cells (PBMC) incubated with and without concanavalin A (ConA) were assayed for cytokine concentrations by enzyme‐linked immunosorbent assay (ELISA).
Results
Significant differences across the four groups were found in the stimulated cellular production of IFN‐γ and IL‐6. Stimulated IFN‐γ production was elevated in the AN group compared to controls. IL‐6 production was significantly elevated in obese subjects relative to the two normal‐weight groups, BN and controls, and tended to be higher in the AN group than in the controls, but not significantly so. IL‐1α production was greater in obese subjects.
Conclusion
The findings of increased IFN‐γ production and a tendency toward increased IL‐6 production (both of which suppress food intake in animals) in individuals who severely restrict food intake suggest a potential role for these cytokines in the pathogenesis of AN. Elevated IL‐6 and IL‐1α production by PBMC in obese individuals requires further investigation to determine if these cytokines contribute to the development or perpetuation of obesity. © 2000 by John Wiley & Sons, Inc. Int J Eat Disord 28: 293–302, 2000. |
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ISSN: | 0276-3478 1098-108X |
DOI: | 10.1002/1098-108X(200011)28:3<293::AID-EAT6>3.0.CO;2-F |