title: Bitter taste and blood glucose are not involved in the suppressive effect of dietary histidine on food intake.
abstract: Histamine decreases food intake by activating histaminergic neurons in the hypothalamus. Histamine is synthesized by histidine decarboxylase (HDC) from histidine. The purpose of this three-part animal study was to clarify the mechanism underlying the suppressive effect of dietary histidine on food intake. In experiment 1, we attempted to distinguish palatability from a direct effect of dietary histidine because histidine tastes slightly bitter to humans. We measured food intake every hour for 24 h in rats fed with a histidine-enriched diet or one of various quinine diets (0.001-0.8% quinine), also bitter. In experiment 2, we measured changes in blood glucose levels in rats fed with a standard or histidine-enriched diet because blood glucose is known to decrease food intake. In experiment 3, we intraperitoneally injected fluoromethylhistidine (FMH), an antagonistic inhibitor of HDC, in rats fed with a histidine-enriched diet. In experiment 1, food intake was almost the same in rats fed with the histidine-enriched diet as that in rats fed with the 0.01% quinine diet until 6 h, but food intake was low in other groups compared with that in the histidine-enriched diet group. After 6 h, food intake did not increase in rats fed with the histidine-enriched diet. In experiment 2, the blood glucose level rose quickly and then began to decrease at approximately 2 h in both groups of rats. However, it decreased more dramatically in rats fed with the histamine-enriched diet and reaches a significant difference from the decrease in the standard-diet group by 6 h. In experiment 3, food intake increased significantly in FMH-injected rats fed with the histidine-enriched diet compared with in non-FMH injected rats. Our results suggest that dietary histidine suppresses food intake by activating histaminergic neurons in the hypothalamus, independently bitter taste and blood glucose level.
authors.affiliation: Department of Health and Nutrition, Bunkyo University Women's College, Kanagawa, Japan.
authors.forename: Kiyoko
authors.initials: K
authors.lastname: Goto
authors.forename: Seiichi
authors.initials: S
authors.lastname: Kasaoka
authors.forename: Miki
authors.initials: M
authors.lastname: Takizawa
authors.forename: Makiko
authors.initials: M
authors.lastname: Ogawa
authors.forename: Takahide
authors.initials: T
authors.lastname: Tsuchiya
authors.forename: Shigeru
authors.initials: S
authors.lastname: Nakajima
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000187:drug effects* / Q000502:physiology; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D004435:Eating / Q000187:drug effects* / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005526:Food, Formulated; D006632:Histamine / Q000378:metabolism*; D006639:Histidine / Q000494:pharmacology*; D006640:Histidine Decarboxylase / Q000037:antagonists & inhibitors / Q000378:metabolism; D007031:Hypothalamus / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009765:Obesity / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D011803:Quinine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013649:Taste / Q000187:drug effects* / Q000502:physiology; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D004791:Enzyme Inhibitors; D006639:Histidine; D006632:Histamine; D011803:Quinine; D006640:Histidine Decarboxylase