TY - JOUR
T1 - Chemical sympathectomy alters food intake and thermogenic responses to catecholamines in rats
AU - Villanueva, Iván
AU - Pión, Manuel
AU - Quevedo-Corona, Lucía
AU - Martínez-Olivares, Rubén
AU - Racotta, Radu
N1 - Funding Information:
This work was partially supported by CGPI-IPN grant # 990169. M. Piñón, L. Quevedo and R. Racotta acknowledge the support of DEDICT-COFAA-IPN. I. Villanueva is fellow of CONACyT.
PY - 2002/7/5
Y1 - 2002/7/5
N2 - It has been suggested that the sympathetic nervous system contributes to the short-term control of feeding. The adrenergic innervation of some splanchnic organs seems to be especially involved in such processes, since catecholamines reduce feeding only when injected intraperitoneally or intraportally. In this work, the effects of neonatal sympathetic denervation with guanethidine (Gnt) upon food intake were assessed in adult rats. Gnt-treated male rats had lower body weight gain. The hypophagic response to intraperitoneal (ip) norepinephrine was 70% higher in Gnt-treated animals as compared to controls (P < 0.05); that of epinephrine (E) by 33% (P < 0.05) and that of isoproterenol was not significantly modified. As in normal rats, the hypophagic effect was much stronger after ip than after intramuscular (im) administration (P < 0.05). On the other hand, resting oxygen consumption (V̇O2) was consistently lower in denervated animals. Ip E administration did not modify V̇O2, while im E caused increased motor activity and V̇O2 (P < 0.05). In contrast to control rats, the respiratory exchange ratio in ad libitum fed Gnt rats did not decrease after Ip E administration, suggesting a lack of effect upon lipid mobilization. The lower rate of body weight gain induced by neonatal Gnt sympathectomy might be due to lower daily food intake possibly related, in part, to the sensitization of the alpha-adrenergic porto-hepatic response to endogenous catecholamines. Compared with controls, Gnt-treated rats also showed a limited thermogenic capacity not related to feeding, and a greater degree of carbohydrate oxidation, possibly due to a defect in E-induced lipolysis, which is beta-adrenergic.
AB - It has been suggested that the sympathetic nervous system contributes to the short-term control of feeding. The adrenergic innervation of some splanchnic organs seems to be especially involved in such processes, since catecholamines reduce feeding only when injected intraperitoneally or intraportally. In this work, the effects of neonatal sympathetic denervation with guanethidine (Gnt) upon food intake were assessed in adult rats. Gnt-treated male rats had lower body weight gain. The hypophagic response to intraperitoneal (ip) norepinephrine was 70% higher in Gnt-treated animals as compared to controls (P < 0.05); that of epinephrine (E) by 33% (P < 0.05) and that of isoproterenol was not significantly modified. As in normal rats, the hypophagic effect was much stronger after ip than after intramuscular (im) administration (P < 0.05). On the other hand, resting oxygen consumption (V̇O2) was consistently lower in denervated animals. Ip E administration did not modify V̇O2, while im E caused increased motor activity and V̇O2 (P < 0.05). In contrast to control rats, the respiratory exchange ratio in ad libitum fed Gnt rats did not decrease after Ip E administration, suggesting a lack of effect upon lipid mobilization. The lower rate of body weight gain induced by neonatal Gnt sympathectomy might be due to lower daily food intake possibly related, in part, to the sensitization of the alpha-adrenergic porto-hepatic response to endogenous catecholamines. Compared with controls, Gnt-treated rats also showed a limited thermogenic capacity not related to feeding, and a greater degree of carbohydrate oxidation, possibly due to a defect in E-induced lipolysis, which is beta-adrenergic.
KW - Epinephrine
KW - Food intake
KW - Guanethidine
KW - Metabolism
KW - Sympathetic nervous system
UR - http://www.scopus.com/inward/record.url?scp=0037025042&partnerID=8YFLogxK
U2 - 10.1016/S0024-3205(02)01739-3
DO - 10.1016/S0024-3205(02)01739-3
M3 - Artículo
SN - 0024-3205
VL - 71
SP - 789
EP - 801
JO - Life Sciences
JF - Life Sciences
IS - 7
ER -