Effect of κ-opiate receptor activation on the levels of insulin, somatostatin and blood glucose in man

The sites of action of several opiate agonists at the feline ileocecal sphincter (ICS) were studied. Dose-response curves for the relatively specific ligands for the mu-, kappa-, and sigma-receptors were determined using morphine (mu-receptors), dynorphin-(1-13) (kappa-receptors), and N-allylnormetazocine (sigma-receptors). Each agonist results in a contractile ICS response. The ICS responded stereospecifically to the levo-isomer of N-allylnormetazocine. Atropine (30 micrograms/kg) or naloxone (100 micrograms/kg) antagonized the ICS response to morphine and to (-)-N-allylnormetazocine. Higher doses of naloxone were required to inhibit the ICS response to dynorphin. Neither atropine nor tetrodotoxin inhibited the ICS response to dynorphin. The ICS response to dynorphin was enhanced after tetrodotoxin. Morphine tachyphylaxis inhibited the ICS response to (-)-N-allylnormetazocine and vice versa. The ICS response to morphine was unaffected by vagotomy but inhibited by trimethaphan camsylate. This study suggests that dynorphin (kappa-receptor) acts at a smooth muscle receptor to mediate contraction and a neural receptor to mediate relaxation, while (-)-N-allylnormetazocine acts at the ICS via a mu-receptor. mu-Receptor activation causes ICS contraction via a cholinergic pathway.

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5-Hydroxytryptamine-induced excitatory postsynaptic currents in neocortical layer V pyramidal cells: suppression by μ-opiate receptor activation

Neuroscience ◽

10.1016/s0306-4522(98)00043-8 ◽

1998 ◽

Vol 86 (2) ◽

pp. 485-497 ◽

Cited By ~ 53

Author(s):

G.J Marek ◽

G.K Aghajanian

Keyword(s):

Pyramidal Cells ◽

Opiate Receptor ◽

Receptor Activation ◽

Excitatory Postsynaptic Currents ◽

Postsynaptic Currents ◽

Layer V ◽

Μ Opiate Receptor

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MiR-7, miR-9 and miR-375 contribute to effect of Exendin-4 on pancreatic β-cells in high-fat-diet-fed mice

Clinical & Investigative Medicine ◽

10.25011/cim.v41i1.29459 ◽

2018 ◽

pp. E16-E24 ◽

Cited By ~ 2

Author(s):

Chang Guo ◽

Yi-Qiong Sun ◽

Qiang Li ◽

Jin-Chao Zhang

Keyword(s):

Blood Glucose ◽

High Fat Diet ◽

Target Genes ◽

Fasting Blood Glucose ◽

Cell Mass ◽

Receptor Activation ◽

Postprandial Blood Glucose ◽

High Fat ◽

Β Cells ◽

Pancreatic Β Cells

Purpose: The purpose of this study was to test whether glucagon-like peptide-1 (GLP-1) receptor activation preserved pancreatic β-cells via the regulation of microRNAs and target genes in high-fat-diet-fed mice. Methods: C57BL/6 male mice were simultaneously treated with high-fat-diet (HFD) and GLP-1 analogue, Exendin-4 (Ex-4) (3 μg/kg/day or 30 μg/kg/day), i.p. or vehicle, for consecutive 13 weeks. Fasting blood glucose, postprandial blood glucose, ΔI30/ΔG30, HOMA-IR and HOMA-% β were measured in each group. Pancreatic β-cell mass was assessed by immunohistochemistry. The expression of miRNAs and related downstream genes were investigated using quantitative real-time PCR. Results: Thirteen weeks of Ex-4 treatment significantly reduced body weight and food intake in HFD-fed mice (P

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