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Hypothalamic histamine regulates feeding suppression induced by 2-deoxy-d -glucose
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ABSTRACTS
Meal patterns of eating disorder and control subjects for multi-item breakfast meals. S. R. SUNDAY and K. A. HALMI. Department of Psychiatry, Cornell UniverSty Medical Coltwe, White Plains, NY, U.S.A.
Meal patterns were examined in anorectic and bulimic patients and restrained and unrestrained controls. All subjects ate a multi-item breakfast meal of scrambled eggs, comflakes in skimmed milk, and sweet rolls. Intake of each food item was monitored continuously by a computer. Hunger, fullness, and urge to eat were rated by subjects at 2-min intervals for 8 min before the meal, throughout the meal, and for 14 min after the meal. Total caloric intake and caloric intake of each of the food items did not differ between the groups but meal duration was significantly longer for anorectics than for the other groups. Anorectics also differed from the other groups in their before meal ratings of hunger, fullness, and urge to eat but not postmeal ratings; additionally, they showed a smaller change in these ratings from the premeal to the postmeal period. Bulimics differed from controls in their perceptions of hunger, fullness and urge to eat in the postmeal but not the premeal period, thus showing a rapid rebound of hunger and a decrement in fullness after eating. Differences between the groups in the microstructure of the meal, in food choice, and cognitions associated with the meal will also be discussed.
Hypothalamic histamine regulates feeding suppression induced by 2-deoxy-D-glucose. Y. TAMARI, M. KUROKAWA, A. OOHARA, H. YOSHIMATSU and T. SAKATA. Department of internal Medicine I, Faculty of Medicine, Kyushu University 71, Fukuoka, 812 and Department of Internal Medicine I, Oita Medical University, Oita, 879-55 Japan.
The central and discrete mechanism involved in delayed suppression of feeding due of 2-deoxy-D-glucose (2-DG) remains unclear, despite its behavioral evidence being so prominent. To clarify the mechanism, we investigated the role of hypothalamic histamine in 2-DGinduced suppression, since glucoprivation is known to release histamine excessively. Infusion of 24 pmol2-DG into the rat third cerebroventricle (icv) decreased food intake for more than 24 h (N = 6, p < 0.01) and lead to initial feeding elicitation. The content of the hypothalamic histamine increased during the period corresponding to the feeding suppression (N =6, p < 0.05). Depletion of neuronal histamine pretreated with a-fluoromethylhistidine, a specific suicide inhibitor of histamine-synthesizing enzyme (histidine decarboxylase), stopped the feeding suppression (N = 6, P < 0.05). The blockage of the postsynaptic site at the histamine neuron was also effective in stopping the suppression through the Hi-receptor (N =6, p
ABSTRACTS
Meal patterns of eating disorder and control subjects for multi-item breakfast meals. S. R. SUNDAY and K. A. HALMI. Department of Psychiatry, Cornell UniverSty Medical Coltwe, White Plains, NY, U.S.A.
Meal patterns were examined in anorectic and bulimic patients and restrained and unrestrained controls. All subjects ate a multi-item breakfast meal of scrambled eggs, comflakes in skimmed milk, and sweet rolls. Intake of each food item was monitored continuously by a computer. Hunger, fullness, and urge to eat were rated by subjects at 2-min intervals for 8 min before the meal, throughout the meal, and for 14 min after the meal. Total caloric intake and caloric intake of each of the food items did not differ between the groups but meal duration was significantly longer for anorectics than for the other groups. Anorectics also differed from the other groups in their before meal ratings of hunger, fullness, and urge to eat but not postmeal ratings; additionally, they showed a smaller change in these ratings from the premeal to the postmeal period. Bulimics differed from controls in their perceptions of hunger, fullness and urge to eat in the postmeal but not the premeal period, thus showing a rapid rebound of hunger and a decrement in fullness after eating. Differences between the groups in the microstructure of the meal, in food choice, and cognitions associated with the meal will also be discussed.
Hypothalamic histamine regulates feeding suppression induced by 2-deoxy-D-glucose. Y. TAMARI, M. KUROKAWA, A. OOHARA, H. YOSHIMATSU and T. SAKATA. Department of internal Medicine I, Faculty of Medicine, Kyushu University 71, Fukuoka, 812 and Department of Internal Medicine I, Oita Medical University, Oita, 879-55 Japan.
The central and discrete mechanism involved in delayed suppression of feeding due of 2-deoxy-D-glucose (2-DG) remains unclear, despite its behavioral evidence being so prominent. To clarify the mechanism, we investigated the role of hypothalamic histamine in 2-DGinduced suppression, since glucoprivation is known to release histamine excessively. Infusion of 24 pmol2-DG into the rat third cerebroventricle (icv) decreased food intake for more than 24 h (N = 6, p < 0.01) and lead to initial feeding elicitation. The content of the hypothalamic histamine increased during the period corresponding to the feeding suppression (N =6, p < 0.05). Depletion of neuronal histamine pretreated with a-fluoromethylhistidine, a specific suicide inhibitor of histamine-synthesizing enzyme (histidine decarboxylase), stopped the feeding suppression (N = 6, P < 0.05). The blockage of the postsynaptic site at the histamine neuron was also effective in stopping the suppression through the Hi-receptor (N =6, p