Mediation of insulin hyperphagia by specific central opiate receptor antagonists.
Mediation of insulin hyperphagia by specific central opiate receptor antagonists.
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通过特定的中枢阿片受体拮抗剂介导胰岛素摄入过多。
DOI:
10.1016/0006-8993(91)90977-4
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发表时间:
1991
期刊:
影响因子:
2.9
通讯作者:
Bodnar,RJ
中科院分区:
文献类型:
--
作者:
Beczkowska,IW;Bodnar,RJ
The hyperphagic properties of insulin (10 U/kg, s.c.) were transiently (2 h) and dose-dependently inhibited (30%) by central pretreatment with naltrexone (20–50 μg, i.c.v.). The irreversible μ opioid antagonist, β-funaltrexamine (B-FNA, 20 μg, i.c.v.) significantly inhibited insulin hyperphagia by 28–54% over the 6-h time course. In contrast, insulin hyperphagia was only transiently (2 h) inhibited (27–30%) by either the irreversibleμ1antagonist, naloxonazine (50 μg, i.c.v.) or the selective κ antagonist, nor-binaltorphamine (NorBNI, 20 μg, i.c.v.). The δ-antagonistic actions of [d-Ala2, Leu5, Cys6]-enkephalin (DALCE, 40 μg, i.c.v.) failed to affect insulin hyperphagia. These data suggest that theμ2opioid receptor subtype modulates insulin hyperphagia.