TY - JOUR
T1 - Glucoprivic feeding is impaired by lateral or fourth ventricular alloxan injection
AU - Ritter, S.
AU - Murnane, J. M.
AU - Ladenheim, E. E.
PY - 1982
Y1 - 1982
N2 - Feeding and blood glucose responses to insulin and 2-deoxy-D-glucose (2-DG) were examined in rats previously given lateral or fourth ventricular injections of the diabetogenic agents, alloxan and streptozotocin. Although streptozotocin (120, 200, and 400 μg) was ineffective, lateral ventricular alloxan injections (40 μg in 5 μl) reduced feeding to 45% of control after 350 mg/kg 2-DG (sc), 33% of control 150 mg/kg 2-DG, and 65% of control after insulin (2 U/kg). Fourth ventricular alloxan injections produced greater deficits, reducing feeding to 19, 7, and 46% of control, respectively. The sympathoadrenal response to glucoprivic agents was normal after alloxan treatment; however, blood glucose levels fell more rapidly during fasting than in controls. Alloxan-induced deficits did not appear to result from damage to catecholamine neurons, since neither regional concentrations nor glucoprivation-induced elevation of catecholamine turnover was altered by alloxan pretreatment. We conclude that cells involved in the glucoprivic control of feeding can be selectively and permanently damaged by intracerebroventricular alloxan administration. Such cells appear to reside in the hindbrain, to be noncatecholaminergic, and to function independently of glucoreceptors mediating sympathodrenal discharge.
AB - Feeding and blood glucose responses to insulin and 2-deoxy-D-glucose (2-DG) were examined in rats previously given lateral or fourth ventricular injections of the diabetogenic agents, alloxan and streptozotocin. Although streptozotocin (120, 200, and 400 μg) was ineffective, lateral ventricular alloxan injections (40 μg in 5 μl) reduced feeding to 45% of control after 350 mg/kg 2-DG (sc), 33% of control 150 mg/kg 2-DG, and 65% of control after insulin (2 U/kg). Fourth ventricular alloxan injections produced greater deficits, reducing feeding to 19, 7, and 46% of control, respectively. The sympathoadrenal response to glucoprivic agents was normal after alloxan treatment; however, blood glucose levels fell more rapidly during fasting than in controls. Alloxan-induced deficits did not appear to result from damage to catecholamine neurons, since neither regional concentrations nor glucoprivation-induced elevation of catecholamine turnover was altered by alloxan pretreatment. We conclude that cells involved in the glucoprivic control of feeding can be selectively and permanently damaged by intracerebroventricular alloxan administration. Such cells appear to reside in the hindbrain, to be noncatecholaminergic, and to function independently of glucoreceptors mediating sympathodrenal discharge.
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U2 - 10.1152/ajpregu.1982.243.3.r312
DO - 10.1152/ajpregu.1982.243.3.r312
M3 - Article
C2 - 6214195
AN - SCOPUS:0020183431
SN - 0363-6119
VL - 12
SP - R312-R317
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 2
ER -