title: Activation of κ-opioid receptor exerts the glucose-homeostatic effect in streptozotocin-induced diabetic mice.
abstract: Opioid and its receptors play important roles in glucose homeostasis. However, few reports were available for the study of κ-opioid receptor in glucose regulation. In our study, we found that the blood glucose of diabetic mice dropped significantly following the treatment with U50,488H (a selective κ-opioid receptor agonist). This phenomenon was time-dependent and associated with the coincident alteration of Glut4 translocation in the skeleton muscles. U50,488H increased the serum adiponectin, but not serum insulin in diabetic mice. U50,488H increased the AdipoR1 expression at both mRNA and protein levels. It also promoted AMPK phosphorylation and Glut4 translocation. All these effects were abolished by nor-BNI (a selective κ-opioid receptor antagonist). These findings suggest that activation of κ-opioid receptor reduces hyperglycemia in streptozotocin-induced diabetic mice. This effect is associated with the translocation of Glut4 and might be relevant to increased adiponectin, AdipoR1, and AMPK phosphorylation.
authors.affiliation: Department of Physiology, National Key Discipline of Cell Biology, Fourth Military Medical University, Xi'an, 710032, Shaanxi Province, China.
authors.forename: Yulong
authors.initials: Y
authors.lastname: Shang
authors.forename: Fan
authors.initials: F
authors.lastname: Guo
authors.forename: Juan
authors.initials: J
authors.lastname: Li
authors.forename: Rong
authors.initials: R
authors.lastname: Fan
authors.forename: Xinliang
authors.initials: X
authors.lastname: Ma
authors.forename: Yuemin
authors.initials: Y
authors.lastname: Wang
authors.forename: Na
authors.initials: N
authors.lastname: Feng
authors.forename: Yue
authors.initials: Y
authors.lastname: Yin
authors.forename: Min
authors.initials: M
authors.lastname: Jia
authors.forename: Shumiao
authors.initials: S
authors.lastname: Zhang
authors.forename: Jingjun
authors.initials: J
authors.lastname: Zhou
authors.forename: Hongbing
authors.initials: H
authors.lastname: Wang
authors.forename: Jianming
authors.initials: J
authors.lastname: Pei
mesh_terms: D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer / Q000494:pharmacology*; D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D052242:Adiponectin / Q000097:blood; D018712:Analgesics, Non-Narcotic / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D015153:Blotting, Western; D003921:Diabetes Mellitus, Experimental / Q000097:blood* / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D006706:Homeostasis / Q000187:drug effects*; D006943:Hyperglycemia / Q000097:blood / Q000517:prevention & control; D007328:Insulin / Q000097:blood; D008297:Male; D008807:Mice, Inbred BALB C; D009271:Naltrexone / Q000031:analogs & derivatives / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D010766:Phosphorylation / Q000187:drug effects; D021381:Protein Transport / Q000187:drug effects; D054419:Receptors, Adiponectin / Q000235:genetics / Q000378:metabolism; D017473:Receptors, Opioid, kappa / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D052242:Adiponectin; D018712:Analgesics, Non-Narcotic; D001786:Blood Glucose; D051275:Glucose Transporter Type 4; D007328:Insulin; D009292:Narcotic Antagonists; D054419:Receptors, Adiponectin; D017473:Receptors, Opioid, kappa; C495693:Slc2a4 protein, mouse; C475419:adiponectin receptor 1, mouse; C051844:norbinaltorphimine; D009271:Naltrexone; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D055372:AMP-Activated Protein Kinases
keywords: ADIPONECTIN; ADIPOR1; AMPK; DIABETES; GLUT4; OPIOIDS