Abstract

<p style="text-align: justify;"><strong>Background:</strong> There is no definitive conclusion on relationship between insulin and pain threshold through opioid mechanism in experimental animal model. The present study investigated the role of endogenous insulin in the modulation of pain using opioid drugs through opioid mechanism and their relationship in experimental animal model. <strong>Methods:</strong> Eight animal groups were used, each group consisting of six mice (Swiss albino). Group 1-treated saline ip; Group 2- administered pentazocine ip; Group 3- treated naloxone in low dose (0.005 mg/kg, ip) 15 min prior to pentazocine treatment; Group 4- administered naloxone in high dose (5 mg/kg, ip)15 min prior to pentazocine treatment. Another four groups of animals (Group 5, 6, 7 and 8) treated saline, pentazocine, low dose and high dose naloxone both administered 15 min prior to pentazocine treatment respectively. Group 1,2,3 and 4 subjected to acetic acid challenge and Group 5,6, 7 and 8 subjected to formalin test. Blood samples were collected and serum insulin was estimated by ELISA and blood glucose was measured by using Ames glucometer. <strong>Results:</strong> Pentazocine significantly increased both serum insulin and antinociceptive response to nociceptive stimuli to acetic acid as well as formalin challenge without significantly affecting plasma glucose in both pain models as compared to saline control. <strong>Conclusion: </strong>The study concluded that possible association between endogenous insulin and pain threshold which is independent of the glycemic status in both the chemically induced nociceptive tests. The relationship between endogenous insulin and pain threshold involves an interaction with opioid system possibly by binding with kappa receptor. <strong>Key words: </strong>Endogenous insulin, Plasma glucose, Pentazocine, Pain thresholds, Mice.

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