Cytokine production in patients with anorexia nervosa, bulimia nervosa, and obesity

Raymond, Nancy C.; Dysken, Maurice W.; Bettin, Kris M.; Eckert, Elke D.; Crow, Scott J.; Markus, Kristy; Pomeroy, Claire

doi:10.1002/1098-108x(200011)28:3<293::aid-eat6>3.0.co;2-f

Cited by 65 publications

(51 citation statements)

References 29 publications

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“…Data regarding pro-inflammatory cytokines in AN are contradictory, with reports of increased [34,35] or normal levels of IL-6 [36][37][38][39][40], normal [36,38,40] or decreased levels of IL-1β [39], and normal [34,36,40] or increased levels of TNF-α [35]. We observed high IL-6 levels in AN, however, IL-6 did not predict BMD or levels of bone markers in our subjects.…”

Section: Hypogonadismcontrasting

confidence: 85%

Anorexia nervosa and osteoporosis

Misra

Klibanski

2006

Rev Endocr Metab Disord

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Anorexia nervosa (AN), a condition of severe undernutrition, is associated with low bone mineral density (BMD) in adults and adolescents. Whereas adult women with AN have an uncoupling of bone turnover markers with increased bone resorption and decreased bone formation markers, adolescents with AN have decreased bone turnover overall. Possible contributors to low BMD in AN include hypoestrogenism and hypoandrogenism, undernutrition with decreased lean body mass, and hypercortisolemia. IGF-I, a known bone trophic factor, is reduced despite elevated growth hormone (GH) levels, leading to an acquired GH resistant state. Elevated ghrelin and peptide YY levels may also contribute to impaired bone metabolism. Weight recovery is associated with recovery of BMD but this is often partial, and long-term and sustained weight recovery may be necessary before significant improvements are observed. Anti-resorptive therapies have been studied in AN with conflicting results. Oral estrogen does not increase BMD or prevent bone loss in AN. The combination of bone anabolic and anti-resorptive therapy (rhIGF-I with oral estrogen), however, did result in a significant increase in BMD in a study of adult women with AN. A better understanding of the pathophysiology of low BMD in AN, and development of effective therapeutic strategies is critical. This is particularly so for adolescents, who are in the process of accruing peak bone mass, and in whom a failure to attain peak bone mass may occur in AN in addition to loss of established bone.

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Section: Hypogonadismcontrasting

confidence: 85%

Anorexia nervosa and osteoporosis

Misra

Klibanski

2006

Rev Endocr Metab Disord

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“…No significant changes were revealed regarding INF-γ concentrations in females with AN [36,39]. However, the production of INF-γ by stimulated peripheral blood mononuclear cells was decreased [57] or elevated in subjects with AN compared to controls [36,37]. To our knowledge, so far there have been no reports on PGE 2 concentrations and the relationship between PGE 2 and bone metabolism in girls with AN.…”

Section: Prace Oryginalnementioning

confidence: 73%

“…However, these investigations were only carried out in young women, the patient groups were small, and the obtained results ambiguous. Raymond et al [37] did not observe significant changes in spontaneous and concanavalin A-induced in vitro TGF-β1 production in peripheral blood mononuclear cells of patients with AN. Pomeroy et al [38] found significant elevation of TGF-β, while Corcos et al [39] found a significant decrease of TGF-β2, in young women with AN compared to the control participants.…”

Section: Prace Oryginalnementioning

confidence: 93%

“…Considering the fact that TGF-β1, a ubiquitous growth factor, is not a pro-but an anti-inflammatory cytokine that controls both osteoblast and osteoclast differentiation, and therefore balances between bone formation and resorption [2,7,8], it might be expected that possible disturbances in its production could have some role in the mechanism leading to the development of osteoporosis in adolescents with AN. Raymond et al [37] investigated spontaneous or mitogen-induced secretion of TGF-β1 from peripheral blood mononuclear cells in patients with AN. There were also clinical studies aimed at determining serum TGF-β1 concentrations [38,39].…”

Section: Prace Oryginalnementioning

confidence: 99%

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TGF-β1, metabolizm kostny, osteoprotegeryna i rozpuszczalny ligand receptora aktywatora czynnika jądrowego-B u dziewcząt z jadłowstrętem psychicznym

Ostrowska

Ziora

Oświęcimska

et al. 2016

Endokrynologia Polska

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Introduction: Numerous investigations, and especially in vitro studies, indicate that TGF-β1 may act as an important regulator of bone remodelling. Thus, it could be expected that disturbances of this cytokine production observed by several researchers might play a role in the mechanism leading to the development of osteoporosis in girls with anorexia nervosa (AN). The aim of the study was to determine whether 1) girls with AN exhibited a relationship between TGF-β1 and bone metabolism (as assessed based on serum OC and CTx concentrations) and 2) whether OPG and sRANKL might modify the possible relationship between TGF-β1 and bone metabolism. Material and methods: Serum concentrations of TGF-β, OC, CTx, OPG, and its soluble ligand sRANKL were determined by ELISA in 60 girls with AN and in 20 healthy controls (C). All study participants were aged 13 to 17 years. Results: Body weight, BMI, BMI-SDS and the Cole index, serum TGF-β1, OC, CTx, and the OPG/sRANKL ratio were significantly reduced, while OPG and sRANKL levels were significantly increased, in girls with AN compared to healthy participants. BMI and the Cole index correlated negatively and significantly with serum CTx and OPG (AN group) or CTx only (groups C and C + AN). Girls with AN showed a positive and significant correlation between the Cole index and serum TGF-β1. The combination group (C + AN) showed a positive and significant correlation between BMI, the Cole index, and the OPG/sRANKL ratio and TGF-β1 concentration, while TGF-β1 correlated positively and significantly with OC concentrations and the OPG/sRANKL ratio. The Cole index and BMI were identified to be significant and independent predictors of CTx (C, AN, and C+AN groups) and OPG (AN group); the Cole index, BMI, and TGF-β1 independently predicted the OPG/sRANKL ratio (C, AN, and C + AN groups); TGF-β1 was found to be an independent predictor of OC (C + AN group). Conclusions: Changes in bone markers, OPG, and/or OPG/sRANKL ratio observed in girls with AN are associated with changes in serum TGF-β1 concentrations. TGF-β1 suppression in girls with AN might lead to disturbances in the relationship between bone metabolism and the OPG/sRANKL system, which, in turn, might compromise the mechanism compensating for bone remodelling disturbances. (Endokrynol Pol 2016; 67 (5): 493-500)

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“…In addition to leptin, TNF-a or IL-6 are potential candidates. TNF-a and IL-6 production in peripheral lymphocytes is reported to be increased both in obese subjects and in patients with anorexia nervosa [24]. However, the exact role of IL-6 production in obese subjects is not known.…”

Section: Discussionmentioning

confidence: 99%

Leptin Regulation of the Thyroids: Negative Regulation on Thyroid Hormone Levels in Euthyroid Subjects and Inhibitory Effects on Iodide Uptake and Na+/I- Symporter mRNA Expression in Rat FRTL-5 Cells

et al. 2004

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Abstract. Leptin receptors are distributed throughout the body and leptin has been shown to have various effects. As we have recently demonstrated a positive correlation between serum leptin levels and TSH in euthyroid subjects, we investigated the effect of leptin on the thyroids. It was observed that serum leptin levels were negatively correlated with free thyroxine/TSH ratios in the serum of euthyroid female subjects. This suggests that leptin may modulate TSH effects. RT-PCR for leptin receptor expression revealed that FRTL-5 cells possess the gene transcript to the long cytoplasmic form of the receptor. Leptin actually appeared to induce an increase in c-fos mRNA expression. However, it inhibited iodide uptake typically induced by both TSH and dibutyryl cAMP, while leptin did not inhibit TSH-induced cAMP production or TSH-stimulated DNA synthesis in 4H medium (in the absence of insulin and TSH). Leptin also was observed to inhibit TSH-and dibutyryl cAMP-induced Na + /I -symporter and thyroglobulin mRNA expression. Lastly, leptin was seen to inhibit TSH-stimulated thymidine incorporation in 5H medium. Taken together, these results suggest that leptin suppresses TSH-induced thyroid function. Therefore, we hypothesized that leptin may be one of the regulators of thyroid function in obese patients. LEPTIN, the gene product of the ob gene, is produced by fat tissues and acts in an endocrine fashion by reporting the size of the adipose tissue mass to hypothalamic leptin receptors that ultimately control the appetite and energy expenditure [1]. Recent studies show that leptin receptors are widely distributed throughout the body and that they have a variety of effects on a number of tissues. For example, functional leptin receptors are expressed in the ovary where leptin mediates the signal between fat storage and the reproductive system [2]. As for the thyroid, we earlier demonstrated a positive relation between serum leptin and TSH levels in euthyroid subjects [3]. In addition to our data, Wesche et al. reported that in obese subjects a larger thyroid size was associated with slightly but significantly higher TSH and lower free thyroxine (fT 4 ) serum levels [4]. As serum leptin concentrations positively correlate with body fat mass or body mass index, serum leptin levels should be higher in the obese subjects. We therefore assumed that leptin stimulates proliferation of thyroid cells or inhibits thyroid hormone synthesis stimulated by TSH in obese subjects by some mechanism. In order to clarify the possible role of leptin in regulation of thyroid function, we first analyzed the relation between serum leptin concentrations and fT 4 /TSH ratio in order to re-confirm the clinical relationship between obesity and thyroid function in euthyroid subjects. Next we investigated the direct actions of leptin on

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Cytokine production in patients with anorexia nervosa, bulimia nervosa, and obesity

Cited by 65 publications

References 29 publications

Anorexia nervosa and osteoporosis

Anorexia nervosa and osteoporosis

TGF-β1, metabolizm kostny, osteoprotegeryna i rozpuszczalny ligand receptora aktywatora czynnika jądrowego-B u dziewcząt z jadłowstrętem psychicznym

Leptin Regulation of the Thyroids: Negative Regulation on Thyroid Hormone Levels in Euthyroid Subjects and Inhibitory Effects on Iodide Uptake and Na+/I- Symporter mRNA Expression in Rat FRTL-5 Cells

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