Modulation by insulin rather than blood glucose of the pain threshold in acute physiological and flavone induced antinociception in mice.
The present study investigated the cause effect relationship between glycemic and algesic states. The hypo- and hyperglycemic conditions were induced physiologically through exercise (3 min swim at room temperature 28 degrees - 30 degrees C) and external dextrose (2 g/kg, ip) administration respectively in mice. Besides, flavone (50 mg/kg, sc) a known antinociceptive drug was chosen to study such a cause effect relationship. The anti-nociception was assessed by acetic acid assay, blood glucose measured using glucometer (Ames) and serum insulin by radioimmunoassay. The findings revealed that irrespective of the glycemic state whether hypo-, hyper, or euglycemic induced by swim stress, dextrose or flavone per se respectively, significant antinociceptive response was recorded. Pretreatment with flavone (50 mg/kg, sc) always exhibited a tendency to reverse the hyperglycemia, if any, but enhanced the antinociceptive response either after swim stress or after dextrose. These data support the contention that changes in the glycemic state in acute condition is not responsible for antinociceptive response and thereby suggesting dissociation between these two parameters. Extended studies estimating serum insulin level after the above mentioned maneuvers showed a significant rise whenever antinociceptive response was recorded irrespective of the glycemic state. It is suggested that serum insulin level, a hormonal parameter rather than the blood glucose level, which is a metabolic parameter, appears more reliable. It appears that the changes in serum insulin level produced by various treatments may have a relationship with the antinociceptive response. However, this study has the limitation that the results can apply only for acute conditions and extrapolation to clinical conditions is debatable.
Rajendran
N N
NN
Institute of Pharmacology, Madras Medical College and Research Institute, Chennai, India.
Thirugnanasambandam
P
P
Parvathavarthini
S
S
Viswanathan
S
S
Ramaswamy
S
S
D019342:Acetic Acid / Q000633:toxicity; D000700:Analgesics / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000502:physiology*; D047309:Flavones; D005419:Flavonoids / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology; D006943:Hyperglycemia / Q000503:physiopathology; D007003:Hypoglycemia / Q000503:physiopathology; D007328:Insulin / Q000502:physiology*; D008297:Male; D051379:Mice; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D010146:Pain / Q000139:chemically induced / Q000503:physiopathology* / Q000517:prevention & control; D017288:Pain Threshold / Q000502:physiology*; D011863:Radioimmunoassay; D013550:Swimming
D000700:Analgesics; D001786:Blood Glucose; D047309:Flavones; D005419:Flavonoids; D007328:Insulin; D009292:Narcotic Antagonists; D009270:Naloxone; D005947:Glucose; D019342:Acetic Acid; C043562:flavone