• Neuroscience letters · Jul 2002

    Nitric oxide production in hypothalamus of 2-deoxy-D-glucose-treated and food deprived mice.

    • Jun Yamada, Hiroshi Hirose, and Yumi Sugimoto.
    • Department of Pharmacology, Kobe Pharmaceutical University, Motoyamakita-machi, Higashinada-ku, Kobe 658-8558, Japan. j-yamada@kobepharma-u.ac.jp
    • Neurosci. Lett. 2002 Jul 19; 327 (2): 107-10.

    AbstractNitric oxide (NO) has been suggested to be involved in the regulation of food intake. In the present study, NO metabolite (nitrite and nitrate, NOx) levels in the hypothalamus were determined in hyperphagic mice. In normal mice, NOx levels were higher in the hypothalamus than those in frontal cortex. Although 2-deoxy-D-glucose (2-DG) is known to induce hyperphagia by inhibiting glucose utilization, it did not affect NOx levels in the hypothalamus of mice. NOx concentration in the hypothalamus decreased in 48 h-food deprived mice. In the frontal cortex, neither 2-DG nor food deprivation affected NOx levels. These results suggest that NO production in the hypothalamus does not increase in 2-DG-elicited hyperphagia and that food deprivation reduces hypothalamic NO, probably by inhibiting NO synthase.

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