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Histidine Suppresses Food Intake through Its Conversion into Neuronal Histamine

Hironobu Yoshimatsu^*, Seiichi Chiba^*, Daisuke Tajima^*, Yuko Akehi and Toshiie Sakata^*,1

^* Department of Internal Medicine I, School of Medicine, Oita Medical University, Hasama, Oita, 879-5593; and
Department of Laboratory Medicine, School of Medicine, Fukuoka University, Fukuoka, Japan

Hypothalamic neuronal histamine has been shown to regulate feeding behavior and energy metabolism as a target of leptin action in the brain. The present study aimed to examine the involvement of L-histidine, a precursor of neuronal histamine, in the regulation of feeding behavior in rats. Intraperitoneal (ip) injection of L-histidine at doses of 0.35 and 0.70 mmol/kg body weight significantly decreased the 24-hr cumulative food and water intakes compared to phosphate buffered saline injected controls (P < 0.05 for each). This suppression of feeding was mimicked dose-dependently by intracerebroventricular infusion of histidine at doses of 0.5, 1.0, and 2.0 µmol/rat (P < 0.05 for each). Pretreatment of the rats with an ip bolus injection of -fluoromethylhistidine, a suicide inhibitor of a histidine decarboxylase (HDC), at a dosage of 224 µmol/kg blocked the conversion of histidine into histamine and attenuated the suppressive effect of histidine on food intake from 64.2% to 88.1% of the controls (P < 0.05). Administration of 0.35 mmol/kg histidine ip increased the concentration of hypothalamic neuronal histamine compared with the controls (P < 0.05). HDC activity was increased simultaneously by histidine administration compared with the controls (P < 0.05). The present findings indicate that L-histidine suppresses food intake through its conversion into histamine in the hypothalamus.

Key Words: L-histidine • hypothalamic neuronal histamine • histidine decarboxylase • feeding behavior

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