Reciprocal modulation of sweet taste by leptin and endocannabinoids

Mayu Niki, Masafumi Jyotaki, Ryusuke Yoshida, Yuzo Ninomiya

Research output: Chapter in Book/Report/Conference proceedingChapter

22 Citations (Scopus)


Sweet taste perception is important for animals to detect carbohydrate source of calories and has a critical role in the nutritional status of animals. Recent studies demonstrated that sweet taste responses can be modulated by leptin and endocannabinoids [anandamide (N-arachidonoylethanolamine) and 2-arachidonoyl glycerol]. Leptin is an anorexigenic mediator that reduces food intake by acting on hypothalamic receptor, Ob-Rb. Leptin is shown to selectively suppress sweet taste responses in wild-type mice but not in leptin receptor-deficient db/db mice. In marked contrast, endocannabinoids are orexigenic mediators that act via CB1 receptors in hypothalamus and limbic forebrain to induce appetite and stimulate food intake. In the peripheral taste system, endocannabinoids also oppose the action of leptin and enhance sweet taste sensitivities in wild-type mice but not in mice genetically lacking CB1 receptors. These findings indicate that leptin and endocannabinoids not only regulate food intake via central nervous systems but also may modulate palatability of foods by altering peripheral sweet taste responses via their cognate receptors.

Original languageEnglish
Title of host publicationSensory and Metabolic Control of Energy Balance
EditorsWolfgang Meyerhof, Hans-Georg Joost, Ulrike Beisiegel
Number of pages14
Publication statusPublished - Oct 14 2010

Publication series

NameResults and Problems in Cell Differentiation
ISSN (Print)0080-1844
ISSN (Electronic)1861-0412

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Cell Biology


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