Intelligence quotient and cognitive functions in severe restricting-type anorexia nervosa before and after weight gain

Plasma concentrations of endothelium-associated proteins (EAP) (plasma fibronectin (PFN), angio-tensin-converting enzyme, factor VIII-related antigen (F VIII-R:Ag)) and tissue plasminogen activator and serum thyroid hormone concentrations were studied in nine patients with anorexia nervosa (AN), before and after weight gain. Before weight gain (-35.9 (se 2.3)% of standard body-weight) PFN was significantly reduced and F VIII-R:Ag was significantly increased in AN patients compared with the concentrations in control subjects (211.5 (se 14.9)v.274.7 (se 16.6) μg/ml,P< 0.05; 129.2 (se 14.1)v.88.2 (se 9.7)%,P<0.05 respectively). Serum triiodothyronine (T3) and free T3 levels were also significantly lower before weight gain in AN patients (0.85 (se 0.07)v.1.53 (se 0.08) nmol/l,P< 0.001; 2.57 (se 0.23)v.5.31 (se 0.34) pmol/l,P< 0.001 respectively), although serum thyroxine (T4), free T4, and thyrotropin concentrations were within the normal range throughout the study periods. Following weight gain, PFN and F VIII-R: Ag concentrations normalized as did the thyroid hormone levels. The incremental changes in PFN levels correlated significantly with those in serum thyroid hormone concentrations (T3,r0.79,P<0.01; free T3,r0.84,P< 0.01). These findings suggest that PFN levels may be directly related to serum T3 concentrations in AN patients.

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Weight gain decreases elevated plasma ghrelin concentrations of patients with anorexia nervosa

Acta Endocrinologica ◽

10.1530/eje-1450669 ◽

2001 ◽

Vol 145 (5) ◽

pp. 669-673 ◽

Cited By ~ 256

Author(s):

B Otto ◽

U Cuntz ◽

E Fruehauf ◽

R Wawarta ◽

C Folwaczny ◽

...

Keyword(s):

Anorexia Nervosa ◽

Weight Gain ◽

Energy Homeostasis ◽

Receptor Subtype ◽

Plasma Samples ◽

Psychotherapeutic Treatment ◽

Ghrelin Receptor ◽

Fasting Plasma ◽

Before And After ◽

Partial Weight

OBJECTIVE: Ghrelin is a new gastric hormone that has been identified as an endogenous ligand for the growth hormone (GH) secretagogue receptor subtype 1a (GHS-R1a). Ghrelin administration however not only stimulates GH secretion but also induces adiposity in rodents by increasing food intake and decreasing fat utilization. We hypothesized that impaired ghrelin secretion in anorexia nervosa may be involved in the pathogenesis of this eating disorder. To examine this hypothesis and to further investigate the role for ghrelin in regulating energy homeostasis, we analyzed circulating ghrelin levels in patients with anorexia nervosa and examined possible correlations with clinical parameters before and after weight gain. METHODS: Plasma ghrelin levels were measured in overnight fasting plasma samples from 36 female patients with anorexia nervosa (age: 25.0+/-1.2 years, BMI: 15.2+/-0.2 kg/m(2)) before and after weight gain following psychotherapeutic treatment intervention in a psychosomatic institution. Plasma ghrelin levels were also measured in fasting plasma samples from 24 age-matched female controls (31+/-1.4 years, BMI: 22.9+/-0.45 kg/m(2)). For quantification of ghrelin levels a commercially available radioimmunoassay (Phoenix Pharmaceuticals, USA) was used. RESULTS: Fasting plasma ghrelin levels in anorectic patients were significantly higher (1057+/-95 pg/ml) than in normal age-matched female controls (514+/-63 pg/ml n=24, P=0.02). Therapeutic intervention in a psychosomatic institution caused an BMI increase of 14% (P<0.001) leading to a significant decrease in circulating ghrelin levels of 25%, (P=0.001). A significant negative correlation between Deltaghrelin and DeltaBMI was observed (correlation coefficient: -0.47, P=0.005, n=36). CONCLUSION: We show for the first time that fasting plasma levels of the novel appetite-modulating hormone ghrelin are elevated in anorexia nervosa and return to normal levels after partial weight recovery. These observations suggest the possible existence of ghrelin resistance in cachectic states such as caused by eating disorders. Future studies are necessary to investigate putative mechanisms of ghrelin resistance such as a possible impairment of intracellular ghrelin receptor signaling in pathophysiological states presenting with cachexia.

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