Oral Administration of D-aspartate, but not of L-aspartate, Reduces Food Intake in Chicks

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  • Erwan Edi
    Laboratory of Regulation in Metabolism and Behavior, Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University, Japan
  • Tomonaga Shozo
    Laboratory of Regulation in Metabolism and Behavior, Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University, Japan Present address : Laboratory of Nutritional Science for Animals, Division of Applied Biosciences, Graduate School of Agriculture, Kyoto University, Japan
  • Ohmori Taketo
    Microbial Genetic Division, Institute of Genetic Resources, Faculty of Agriculture, Kyushu University, Japan
  • Mutaguchi Yuta
    Microbial Genetic Division, Institute of Genetic Resources, Faculty of Agriculture, Kyushu University, Japan
  • Ohshima Toshihisa
    Microbial Genetic Division, Institute of Genetic Resources, Faculty of Agriculture, Kyushu University, Japan
  • Nagasawa Mao
    Laboratory of Regulation in Metabolism and Behavior, Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University, Japan
  • Yasuo Shinobu
    Laboratory of Regulation in Metabolism and Behavior, Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University, Japan
  • Tamura Yoshinaga
    Asahi Kasei Chemicals Corporation, Japan
  • Furuse Mitsuhiro
    Laboratory of Regulation in Metabolism and Behavior, Graduate School of Bioresource and Bioenvironmental Sciences, Kyushu University, Japan

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In the present study, we determined the effects of oral administration of L- and D-aspartate (L-Asp and D-Asp) on food intake over a period of 2 h after the administration, as well as its effects on the concentration of L- and D-Asp in the brain and plasma. Chicks were orally administered different levels (0, 3.75, 7.5 and 15 mmol/kg body weight) of L-Asp (Experiment 1) and D-Asp (Experiment 2). Administration of several doses of L-Asp linearly increased the concentration of L-Asp, but not of D-Asp, in plasma. Oral L-Asp somewhat modified the levels of L- and D-Asp levels in the telencephalon, but not in the diencephalon. However, food intake was not significantly changed with doses of L-Asp. On the other hand, D-Asp strongly and dose-dependently inhibited food intake over a period of 2 h after the administration. Oral D-Asp clearly increased D-Asp levels in the plasma and diencephalon, but no significant changes in L-Asp were detected. Brain monoamine contents were only minimally influenced by L- or D-Asp administration. We conclude that D-Asp may act as an anorexigenic factor in the diencephalon.

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