Interaction between serum leptin levels and hypothalamo-hypophyseal-thyroid axis in patients with anorexia nervosa
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Pituitary Gland physiology MeSH
- Hypothalamus physiopathology MeSH
- Body Mass Index MeSH
- Insulin-Like Growth Factor I analysis MeSH
- Leptin analysis MeSH
- Humans MeSH
- Anorexia Nervosa physiopathology MeSH
- Neuropeptide Y blood MeSH
- Serotonin blood MeSH
- Thyroid Gland physiopathology MeSH
- Thyroxine blood MeSH
- Triiodothyronine, Reverse blood MeSH
- Triiodothyronine blood MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Insulin-Like Growth Factor I MeSH
- Leptin MeSH
- Neuropeptide Y MeSH
- Serotonin MeSH
- Thyroxine MeSH
- Triiodothyronine, Reverse MeSH
- Triiodothyronine MeSH
The main objective of the study was to evaluate the endocrinological picture of anorexia. Serum leptin levels are low in untreated anorexia nervosa (AN), but studies of the exact relationship between leptin, body weight and hormones of hypothalamo-hypophyseal-thyroid axis and the impact of refeeding in anorectics are limited. The sample consistent of 15 patients with anorexia nervosa before and 1 month after partial weight recovery, and 15 age-matched control subjects. The body mass index (BMI), leptin, plasma neuropeptide Y (NPY), serotonin, thyroxine (T4), triiodothyronine (T3) and reverse triiodothyronine (rT3) in serum were evaluated for each subject. The mean serum levels of leptin, T4, and T3 were significantly lower before weight recovery in 15 patients with AN than they were in control subjects. After partial weight recovery, basal T3 levels were unchanged and significantly lower than in controls. Basal T4 was even still more reduced, but we observed significantly elevated ratio of T3/T4 and reduced ratio rT3/T4 of in AN patients after gain recovery, indicating increased conversion of T4 to T3 than to rT3. The levels of serum leptin were low in AN, but after partial weight recovery slightly increased, and correlated with BMI. No differences were observed in serum NPY. Serum levels of IGF-1 and serotonin were lower in AN than in controls before and after partial weight gain. IGF-1 was slightly increased after partial weight gain. We did not find correlation between serum levels of leptin and serum T4. The low serum levels of T3 associated with chronic starvation were thought to be the result of impaired peripheral conversion of T4 to T3. However, decreased levels of T3 were still apparent even after a partial weight gain, and the concentration of T4 was even lower. The diminished serum level of TSH in AN, however, appeared to return to the level of controls. On the basis of these results, we assume that low serum levels of thyroid hormones in AN reflect a dysfunction of the HPT axis in AN patients. It is known that in man serum serotonin levels correlate positively with T3 levels. It is possible that the low serum levels of thyroid hormones in AN subjects result in low serum serotonin and its product, melatonin. While IGF-1 reflects the energy intake of the previous few weeks, the serum leptin concentration reflects the true status of the adipose stores, a fact that has useful clinical implications.
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