Satiety effect and sympathetic activation of leptin are mediated by hypothalamic melanocortin system

Noriko Satoh, Yoshihiro Ogawa, Goro Katsuura, Yoshito Numata, Hiroaki Masuzaki, Yasunao Yoshimasa, Kazuwa Nakao

Research output: Contribution to journalArticle

175 Citations (Scopus)

Abstract

Leptin is an adipocyte-derived blood-borne satiety factor that decreases food intake and increases energy expenditure, thereby leading to a substantial decrease in body weight. To explore the possible roles of the hypothalamic melanocortin system in leptin action, we examined the effects of intracerebroventricular (ICV) injection of leptin with or without SHU9119, a potent antagonist of α-melanocyte stimulating hormone, on food intake, body weight, and mitochondrial uncoupling protein-1 (UCP-1) mRNA expression in the brown adipose tissue (BAT) in rats. A single ICV injection of leptin decreased cumulative food intake and body weight gain, and increased UCP-1 mRNA expression during 3 h at the onset of the dark phase. Inhibition of food intake and body weight change with leptin was reversed by co-injection of SHU9119 in a dose-dependent manner. Co-injection of SHU9119 also inhibited completely the leptin-induced increase in UCP-1 mRNA expression in the BAT. Treatment with SHU9119 alone did not affect food intake, body weight, and UCP-1 mRNA expression in rats. The present study provides evidence that the hypothalamic melanocortin system plays a central role in both satiety effect and sympathetic activation of leptin.

Original languageEnglish
Pages (from-to)107-110
Number of pages4
JournalNeuroscience Letters
Volume249
Issue number2-3
DOIs
Publication statusPublished - Jun 19 1998
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Satiety effect and sympathetic activation of leptin are mediated by hypothalamic melanocortin system'. Together they form a unique fingerprint.

  • Cite this