Signals from intra-abdominal fat modulate insulin and leptin sensitivity through different mechanisms: Neuronal involvement in food-intake regulation

Tetsuya Yamada, Hideki Katagiri, Yasushi Ishigaki, Takehide Ogihara, Junta Imai, Kenji Uno, Yutaka Hasegawa, Junhong Gao, Hisamitsu Ishihara, Akira Niijima, Hiroyuki Mano, Hiroyuki Aburatani, Tomoichiro Asano, Yoshitomo Oka

研究成果: Article査読

101 被引用数 (Scopus)

抄録

Intra-abdominal fat accumulation is involved in development of the metabolic syndrome, which is associated with insulin and leptin resistance. We show here that ectopic expression of very low levels of uncoupling protein 1 (UCP1) in epididymal fat (Epi) reverses both insulin and leptin resistance. UCP1 expression in Epi improved glucose tolerance and decreased food intake in both diet-induced and genetically obese mouse models. In contrast, UCP1 expression in Epi of leptin-receptor mutant mice did not alter food intake, though it significantly decreased blood glucose and insulin levels. Thus, hypophagia induction requires a leptin signal, while the improved insulin sensitivity appears to be leptin independent. In wild-type mice, local-nerve dissection in the epididymis or pharmacological afferent blockade blunted the decrease in food intake, suggesting that afferent-nerve signals from intra-abdominal fat tissue regulate food intake by modulating hypothalamic leptin sensitivity. These novel signals are potential therapeutic targets for the metabolic syndrome.

本文言語English
ページ(範囲)223-229
ページ数7
ジャーナルCell Metabolism
3
3
DOI
出版ステータスPublished - 2006 3
外部発表はい

ASJC Scopus subject areas

  • 生理学
  • 分子生物学
  • 細胞生物学

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