Hyperphagia of hyperthyroidism: Is neuropeptide Y involved?

Erika Pétervári, Márta Balaskó, Andrea Jech-Mihálffy, Miklós Székely

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The possible role of neuropeptide Y (NPY) was studied in rats with hypermetabolism and hyperphagia induced by thyroxine (50-100-200 μg/day s.c. for 3-4 weeks). Both metabolic rate and body temperature increased quickly with thyroxine treatment, while hyperphagia started to develop only after 2 weeks of treatment. The weight gain rate progressively decreased or stopped. The NPY-induced hyperphagia was not altered significantly during thyroxine treatment (in severe thyrotoxicosis it was rather suppressed); the fasting-induced hyperphagia was smaller than in controls following 1 week of treatment, and it became enhanced only after 3 weeks, when the deficit in body weight indicated a certain level of starvation already prior to the food deprivation. The NPY-antagonist D-Tyr27,36,D-Thr32-NPY(27,36) suppressed this fasting-induced hyperphagia, suggesting that endogenous NPY is involved in this late phase. In conclusion, hyperthyroidism per se does not increase the NPY activity, instead the quickly developing hyperthermia may inhibit the NPY actions; NPY may, however, be activated by a concurrent hypermetabolism-induced starvation.

Original languageEnglish
Pages (from-to)103-110
Number of pages8
JournalRegulatory Peptides
Volume131
Issue number1-3
DOIs
Publication statusPublished - Nov 15 2005

Keywords

  • Body temperature
  • Body weight
  • Fasting
  • Food intake
  • Neuropeptide Y
  • Thyroxine

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Endocrinology
  • Clinical Biochemistry
  • Cellular and Molecular Neuroscience

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